Journées de l’Ecole Doctorale

Physiologie, Physiopathologie et Thérapeutique

Centre de Recherche des Cordeliers

25th and 26th

May, 2016

ACKNOWLEDGMENTS

The organizers would like to thank the following sponsors and exhibitors for their

time and financial support.

The Organizers would also like to thank all of the chairmen and chairwomen, the

conference speakers, and the jury members, for their implication and essential

presence, and for inspiring us with professionalism.

Our warmest thanks also to the Doctoral School’s directors, Pr. Isabelle Cremer

and Dr. Catherine Monnot and the administrator, Mrs Dominique Belle, for their

guidance and unwavering support.

SCIENTIFIC PROGRAM

Wednesday, 25th May, 2016

8:30-9:00 WELCOMING OF PARTICIPANTS

9:00-9:15 INTRODUCTION

Pr. Isabelle CREMER - ED394 director

Dr. Catherine MONNOT - ED394 deputy director

9:15-10:15 PLENARY SESSION I: ONCOLOGY Chair: Yann-Alexandre VANO - Georges Pompidou European Hospital

Adem BOKHARI (UMRS 938, Saint-Antoine Hospital) - Aberrant Splicings due to

Microsatellite Instability in Cancer: Physiopathological role of HSP110 mutation in

colorectal cancer

Benoît USUNIER (IRSN) – Mesenchymal stem cell therapy reduces fibrosis induced

by abdomino-pelvic radiotherapy

Marion CLASSE (Pitié Salpêtrière Hospital) - Molecular characterization of olfactory

neuroblastomas

Maurice ZAOUI (UMRS 938 - UPMC) - Reciprocal changes in gene expression

profiles of cocultured breast cancer cells and adipocytes

10:15 -10:30 POSTER TEASING – FIRST SESSION

10:30 -11:45 POSTER PRESENTATION (1ST SESSION) / Coffee break and Sponsors' visit

11:45 -12:45 PLENARY SESSION II: NEUROLOGY & VISION Chair: Gaël ORIEUX - Institut de la Vision

Hugo CHARLES-MESSANCE (UMRS 968 - Institut de la Vision)

Mononuclear phagocytes induce IL-1β dependent photoreceptor toxicity

Linda HANBOUCH (UMRS 1127 - Institut du Cerveau et de la Moelle)

Mutations at the cholesterol binding site on Amyloid precursor protein modifies

the secretion of amyloid peptides from transfected HEK293T cells

Emily QUENTIN (UMRS 839 - Institut du Fer à Moulin)

CIPPscaffoldprotein :anewinteractorofC-terminal5-HT2Bserotonergic

receptorpromotesignalingpathwayactivity

Emilie SIMONNET (Collège de France) - RoleofEphrine-A4 in the development

and in the physiology of arterial innervation

12:45-14:00 LUNCH BREAK AND SPONSORS’ VISIT

14:00-15:15 LIVE ROUND TABLE DISCUSSION “SCIENTIFIC COMMUNICATION” (French language / en français) Ange ANSOUR – Educational Coordinator “Les Savanturiers”

Mathieu BUONAFINE – Winner of “My Thesis in 180 Seconds”

Anne NASSIF – "Nutrimedia" director

Séverine CIANCIA – Head of Press Inserm Service

Noémie NAGUET – "l'Esprit Sorcier" ("C'est pas sorcier" new version)

15:15-15:30 POSTER TEASING – SECOND SESSION

15:30-16:45 POSTER PRESENTATION (2ND SESSION) / Coffee break and Sponsors' visit

16:45-18:30 PLENARY SESSION III: PATHOPHYSIOLOGY

Chairs: Philippe LE ROUZIC - Saint-Antoine & Gilles CRAMBERT – CRC Mathieu BUONAFINE (UMRS 1138 - CRC) – Implication of the Neutrophil

Gelatinase-Associated Lipocalin (NGAL) from immune cells in aldosterone

induced cardiovascular remodeling

Olivier CLAUDE (UMRS 1166 - ICAN) – Identification of selective adult cardiac

progenitor cells (CPCs) surface markers by proteogenomics approaches

Irma Karen LOPEZ CAYUQUEO (UMRS 970) - Knockin of HA-tagged K+ channel

Kir7.1 as a tool to determine its segmental and subcellular localisation in mouse

kidney.

Ahmad MASSARWEH (UMRS 1149 - UPMC) – Golgi Dolichol linked Oligosaccharide

(DLO) Diphosphatase, a potential regulator of DLO metabolism

Meriam NEFLA (UMRS 938 - Saint-Antoine) – The proinflammatory cytokine 14-3-3ε

is a ligand of CD13 in cartilage.

Benjamin VALLIN (UMRS 8256 - UPMC) – Identification of a new adenylyl cyclase 8

(AC8) isoform: implication in vascular smooth muscle cells (VSMCs)

transdifferentiation and pathological vascular remodeling

Thursday, 26th May, 2016

9:00-10:00 PLENARY SESSION IV: IMMUNOLOGY & INFLAMMATION Chair: Catherine SAUTÈS-FRIDMAN – CRC

Mélanie CRON (UMRS 974 - Pitié-Salpêtrière Hospital) – Characterization of the role

of miR-150 in autoimmune Myasthenia Gravis

Clément LEVIN (CIMI - Pitié-Salpêtrière Hospital) – Role of skin migratory antigen-

presenting cells in T follicular helper cell polarization after intradermal vaccination

Anastasia MIKHAILOVA (Institut Pasteur) – The role of Tuba protein in the dynamics

of immune synapse formation

Emmanuel STEPHEN-VICTOR (UMRS 1138 - CRC) - Cellwallα-(1,3)-glucanfrom

Aspergillus fumigatus induces PD-L1 expression on human dendritic cells that

regulates Th1 and regulatory T cell responses

10:00-10:15 POSTER TEASING – THIRD SESSION

10:15-11:30 POSTER PRESENTATION (3RD SESSION) / COFFEE BREAK AND SPONSORS' VISIT

11:30-12:30 PLENARY SESSION V: VIROLOGY Chair: Olivier SCHWARTZ – Institut Pasteur

Iratxe DEL RIO (Institut Pasteur) - HIV-1 modulation of the T cell activation

molecular machinery

Olivier LUCAR (CIMI - Pitié-Salpêtrière) – New Family of Neutralizing Antibodies in

HIV Asymptomatic Long-Term Non-Progressors

Angeline ROUERS (CIMI - Pitié-Salpêtrière Hospital) – Follicular helperT cells (Tfh)

and memory B cell response during HIV-1 infection

Zineb SBIHI (CIMI - Pitié-Salpêtrière Hospital) – iNKT and Memory B cells deficiency

in HHV-8 Multicentric Castleman Disease

12:30-14:00 LUNCH BREAK AND SPONSORS’ VISIT

14:00-15:00 “SCIENTIFIC INTEGRITY” LECTURE BY PR. PIERRE CORVOL

(French language / en français)

15:00-16:00 PLENARY SESSION VI: METABOLISM & NUTRITION

Chairs: Ghislaine GUILLEMAIN & Armelle LETURQUE – CRC Mengyue HU (UMRS 1138 - CRC) - The role of receptor activator of NF-kB (RANK)

and its ligand (RANKL) in the Non-Alcoholic Fatty Liver Disease(NAFLD)

Cécilia LANDMAN (UMRS 1157 - UPMC) – The N-acyl-homoserine lactone 3-oxo-

C12, an inter-bacterial signaling molecule (involved in quorum sensing), exerts

effects on the host: thus implicating quorum sensing in Inflammatory Bowel

Disease

Ludovica MARINELLI (FInE team - MICALIS, INRA Jouy-en-Josas) - Activation of the

AhR signal pathway by the gut microbiota

Hedi SOUSSI (UMRS 1166 - ICAN) – DAPK2 down-regulation associates with

attenuated adipocyte autophagic clearance in human obesity

16:00-16:15 POSTER TEASING – FOURTH SESSION

16:15-17:30 POSTER PRESENTATION (4TH SESSION), COFFEE BREAK AND SPONSORS' VISIT

17:30-19:00 CLOSING CEREMONY OF THE 17TH JEDS AND AWARDING OF THE PARTICIPANTS -

COCKTAIL

ORAL COMMUNICATIONS - 25th May 2016

Oncology

Adem BOKHARI, Ada Collura, Alex Duval - Aberrant Splicings due to Microsatellite

Instability in Cancer : Physiopathological role of HSP110 mutation in colorectal cancer.

UMRS 938, Saint-Antoine Hospital

Microsatellite instability (MSI) results from impaired DNA mismatch repair, being associated with a

frequent subset of human neoplasms. In the lab, we recently identified the first mutation

affecting a chaperone in human cancer. MSI affects a T17 intronic DNA repeat, located in the

splice acceptor site of HSP110 intron 8 in MSI colorectal cancer (CRC) and leads to aberrant

skipping of exon 9 and the apparition of a premature codon stop (PTC) in the exon 10, resulting

of a mutant protein, referred to as HSP110DE9. We demonstrate that HSP110DE9 interacts with

wild-type HSP110, antagonizing its chaperone activity (dominant negative effect). Moreover, the

overexpression of HSP110DE9 increases the sensitivity of CRC cells to anti-cancer agents and

HSP110 T17 status predicts the relapse-free survival of MSI CRC patients treated with adjuvant

chemotherapy.

In line with these results, the first axis of my PhD project focus to investigate the

pathophysiological consequences of HSP110 mutation in CRC. In our work, now submitted, we

reported that HSP110 induces colon cancer cell proliferation via STAT3 activation, specifically an

increase in STAT3 phosphorylation, nuclear translocation and transcription factor activity. Thus,

the frequent inactivating mutation of this chaperone is probably an important event underlying

the improved prognosis of colon cancer displaying MSI.

In a second work in progress to submission, we study the NMD (Nonsense-mediated mRNA

decay) system as a therapeutical target for MSI CRC. NMD is responsible for the degradation of

mutant mRNAs containing a PTC. We hypothesized that inhibition of NMD activity could be of

particular therapeutic interest for MSI tumors leading to increase of HSP110DE9 protein level.

Using Amlexanox, an approved drug used in clinic, we were able to block the degradation of

HSP110DE9 transcript. Interestingly, systemic administration of this drug led to growth inhibition of

MSI CRC xenografts, but not of microsatellite stable.

Benoît USUNIER, BrunoL’Homme,RadiaTamarat,MarcBenderitterand AlainChapel

– Mesenchymal stem cell therapy reduces fibrosis induced by abdomino-pelvic

radiotherapy.

InstituteofRadiologicalProtection and Nuclear Safety, RadioProtection and Human Health Division,

Fontenay-aux-Roses, France

Theabdomino-pelvicareacontainsthemainorgansatriskforcancer (prostate, colon-

rectum, cervix…). Treatmentprotocolsofteninclude radiotherapy which, while effective for

sterilization of thetumor, cancauseseverelatecomplications, such as fibrosis. During such

treatment, colon andrectumareespecially susceptible to side effects, due to their rapid self-

renewal. There currentlyexistsnoreliabletherapy against fibrosis. Seeinghow Mesenchymal

Stem Cell (MSC) hasproveneffectivein treating radiation injuries, weaimed at

investigatingtheir abilityto reduce radiation-inducedfibrosis to thecolon and rectum. Invivo,

weevaluatedthe effectsofMSC transplantationin rats. We usedasingle dose 29 Gy

colorectal irradiation model on Sprague-Dawley rats. This model produces damages similar

tothelate severelesions observed inradiotherapy patients. MSCswere injected intravenously

atdifferenttime points after radiationexposure to studytheefficacy of cell therapy

priorandafter fibrosisonset. MSCs wereable to reduce fibrosisinboth these situations,

mainlythroughthe inhibitionof inflammatory pathways and thereduction of myofibroblast

activation.Keymediators ofthe effect ofMSCshavebeen identified during this study.

Themodificationofmacrophage polarization towards theM2 phenotypeis induced by

MSCsin vivoand appears to play a major role in their antifibrotic effects. To further understand

the mechanisms underlyingtheseeffects, wesetupna invitro model of myofibroblast

activation. Intestinalfibroblasts andsmooth muscle cells, themainpro-fibrotic cells

inthecolon, were irradiated toinduce changes similar to thoseobservedinvivo. When

cocultured with MSCs, we observed adecreaseinprofibrotic proteins secretionbythese cells.

TheseresultssuggestthatMSC therapyrepresents a promising strategyin the treatment

ofsevereenteritis, rectitisinducedbyradiotherapy of prostate, bladder,uterus cancers.

Marion CLASSE1-3, Xaoping Su2, Michel Wassef3, Frederic Allanic1, Roger Mouawad1,

Benjamin Verillaud4, Geoffrey Mortuaire5, Philippe Herman4, Gabriel Malouf1 and David

Khayat1 - Molecular characterization of olfactory neuroblastomas. 1Département d’ Oncologie Médicale, Groupe Hospitalier Pitiié Salpêtrière, Assistance Publique Hôpitaux

de Paris, Faculté de Médecine Pierre et Marie Curie, Institut Universitaire de Cancérologie GRC5, Université

Paris 6, Paris, France. 2Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer

Center, Houston, Texas, USA. 3Département de Pathologie, Hôpital Lariboisière, Assistance Publique Hôpitaux de Paris, Paris, France. 4Département de chirurgie ORL, Hôpital Lariboisière, Assistance Publique Hôpitaux de Paris, France 5Département de chirurgie ORL, CHRU de Lille, France.

Background: olfactory neuroblastomas (ONBs) are rare tumors arising in the skull base, thought

to develop from neuronal or basal cells of olfactory mucosa. They are traditionally classified into

4 grades according to Hyams grading system which is subjective and poorly reproducible.

Recent studies suggest a simplified classification into low and high grade but no objective

argument has been proved. The goal of our work was to determine a molecular profile of ONBs

compared to normal sinonasal mucosa and to other sinonasal cancers, in order to confirm their

nature and to highlight objective elements to draw the foundations of a new classification

system.

Materiel and methods: we performed RNA next-generation sequencing on 18 ONBs, 1 sinonasal

neuroendocrine carcinoma (SNEC), 3 squamous cell carcinomas (SCCs), 3 intestinal type

adenocarcinomas (ITACs) and 4 normal sinonasal mucosa cryopreserved samples retrieved

from Lariboisière-APHP and Lille-CHRU Pathology departments. All cases were reevaluated and

reclassified if necessary by 2 pathologists.

Results: Unsupervised clustering of gene expression revealed 2 groups. The first group was

composed of normal samples which clustered together, SCCs and ITACs which clustered

according to their histological type and 1 ONB which clustered with SCCs. The second group

was composed of ONBs and the SNEC. Two sub-groups of ONBs were identified. Some of the

most differently overexpressed RNAs in ONBs compared to carcinomas were related to neuronal

differentiation and AKT signaling pathway.

Conclusion: RNA sequencing proves ONBs have a gene expression profile very different from

sinonasal carcinomas and confirms their neuronal differentiation. It also brings molecular

elements to support a low grade – high grade distribution of ONBs. Closer analysis of the 2 ONBs

gene expression subgroups will highlight potential immunohistochemical and therapeutic targets

in order to improve diagnostic and classification, and open new therapeutic paths.

Maurice ZAOUI1,2,3, Nathalie Ferrand1,2,3, Annette K. Larsen1,2,3, Véronique Béréziat1,2,4

and Michèle Sabbah1,2,3 - Reciprocal changes in gene expression profiles of cocultured

breast cancer cells and adipocytes. 1UPMC Univ Paris 06, UMR-s 938, F-75005, Paris, France, 2INSERM UMR_S 938, Centre de recherche Saint-

Antoine, Paris, France. 3Cancer Biology and Therapeutics, Centre de Recherche Saint-Antoine, Paris,

France. 4Genetics and acquired lipodystrophies, Centre de Recherche Saint-Antoine, Paris, France.

Breast cancer is a frequent disease, affecting about one woman out of eight at some time of

life. Epidemiologic data have shown a strong correlation between obesity and increased risk of

breast cancer. Until now, little attention has been paid to the surrounding adipose tissue,

although recent data suggest for instance that adipocytes, under the influence of tumor cells

factors, can contribute to different stages of carcinogenesis. A critical step in tumor growth and

metastasis is tumor vascularization through angiogenesis pathway, which can be activated

directly or under hypoxic circumstances.

We first characterize, as a function of adipocyte stroma modifications, the vasculogenic profile

of epithelial or mesenchymal breast cancer cells. Then the influence of the adipocytes on this

vasculogenic profile.

The studies were conducted using Transwell where murine adipocyte cell line 3T3F442A were not

in direct contact with epithelial (MCF-7) or a mesenchymal (MCF7-sh-WISP2) breast cancer cell

lines . Then the genes and proteins expression levels of vasculogenic and hypoxic factors were

analyzed by QRT-PCR, Western-Blot and ELISA.

First, we observed different angiogenic profile between the epithelial and mesenchymal cell

lines. The MCF-7 cells showed a low VEGF-A, VEGF-C and NRP-1 expression while the

mesenchymal variant presented high levels of these factors. We compared the expression of HIF

(Hypoxia Induced Factor) and we found that mesenchymal cells expressed a higher level of

HIF1α but a lower of HIF1β compared to epithelial cells.

We then observed an increase of VEGF-A and VEGF-C secretion in both tumoral cell lines when

cocultured with adipocytes, while NRP-1 seemed unaffected. There was no effect when the

tumoral cells were cocultured with preadipocytes.

These data suggest that adipocytes can increase angiogenic properties of breast tumoral cells

by increasing their secretion of VEGF-A and VEGF-C leading to a more invasive and metastatic

tumor phenotype.

Neurology & Vision

Hugo CHARLES-MESSANCE1, Chiara Eandi1,2, Lourdes Siqueiros1,Alvaro Rendon1, Ramin

Tadayoni1,3, Florian Sennlaub1 and Xavier Guillonneau1 - Subretinal mononuclear

phagocytes induce IL-1β dependent photoreceptor toxicity 1SorbonneUniversités,UPMCUnivParis06,INSERM,CNRS,Institutdela Vision, 17 rue Moreau, 75012,

Paris, France 2UniversityofTorino, DepartmentofClinicalPhysiopathology,EyeClinic, Torino, Italy 3Serviced'Ophtalmologie,HôpitalLariboisière,AP-HP,DiderotUnivParis 07, Sorbonne Paris Cité, 2 rue

Ambroise Paré,75010,Paris,France

Age-related macular degeneration (AMD) is the leading cause of vision impairment in elderly: it

ischaracterizedbythedegenerationofthe photoreceptor cells in the macula, resulting

inaprogressivelossofcentral vision. AMD is associated with an infiltration and

chronicsubretinal accumulation of mononuclear phagocytes (MPs), among which monocytes

(Mos) andmicroglialcells.WehavepreviouslyshowninanAMDmodelthat subretinal

MosproduceIL-1βandthatIL-1βplaysakeyrolein Cx3cr1-/- Mos photoreceptor

(PR)toxicity.Tofurtherunderstandtherole ofIL-1β inPRtoxicity, we cultured mice retina in

thepresenceofIL-1βor Mos.After18hofculture, explantswere fixed and submitted to

TUNEL labelling or immunostained to label cone PR outer segment. We show that exogenous IL-

1β induced rod PR cell death and that antagonizing glutamate receptor reduces

rodPRcelldeath.InthepresenceofIL-1β, the number of cone PR was not affected

butastrongconesegmentlosswas observed. Similar results have been successfully

reproducedbyculturing retinalexplants with human or Cx3cr1-/- Mos. Our results indicatethat

subretinalMPs inducesevereIL-1β dependent rod and cone toxicity. We will further decipher

the molecular mechanism by which IL-1β impaired photoreceptor functions.

Linda HANBOUCH1, Catherine Marquer1, Gaëlle Fontaine1, Julien Moreau2, Nicolas Gilles3,

Caroline Louis4, Mark J. Millan4 and Marie-Claude Potier1 - Mutations at the cholesterol binding

site on Amyloid precursor protein modifies the secretion of amyloid peptides from transfected

HEK293T cells 1Institut du Cerveau et de la Moelle (ICM), CNRS UMR7225, INSERM UMR_S1127, UPMC, Hôpital Pitié-Salpêtrière, 47, Bd de

l’Hôpital 75013 Paris, France; 2Laboratoire Charles Fabry, Institut d’Optique Graduate School, Université Paris Sud, 2 avenue Augustin Fresnel, 91127

Palaiseau France; 3Centre de recherche du CEA/DSV/iBiTec-S/SIMOPRO Toxins, Receptors and Channels team. Saclay, Bat 152,91191 Gif

sur Yvette; 4Pôle d'Innovation Thérapeutique en Neuropsychiatrie, Institut de Recherches Servier, 125 chemin de Ronde, 78290

Croissy-sur-Seine France

Cholesterol levels are elevated in the brains of Alzheimer’s disease (AD) patients. An increase in

cholesterol at the plasma membrane promotes an increase of endocytosis of the amyloid

precursor protein (APP) leading to an increase of Aβ production. Moreover, an interaction

between C99, the protein fragment resulting from the cleavage of APP by BACE1, and

cholesterol has recently been described. In the present work, we studied the involvement of the

cholesterol-binding site (CBS) on APP endocytosis and the production of amyloid-β peptides

(Aβ).

Mutants of the CBS on APP751-mCherry were constructed using site-directed mutagenesis:

E693K, S697A, K699A, K699E, G700A, G704A, V710A, S697A/K699A and G700A/G704A (numbering

APP770). HEK293T cells were transfected with these mutants and the amounts of intracellular and

extracellular Aβ peptides were measured using ELISA and the MesoScale Discovery 24 hours

after transfection. In parallel, immunostaining of EEA1, a marker of early endosomes, was

performed to quantify the number and size’s endosomes. Surface Plasmon Resonance (SPR) was

used to quantify the interaction between 25aa peptides corresponding to wild-type (wt) or

mutated APP CBS and liposomes containing cholesterol.

All mutants, except S697A, produced very low levels of secreted Aβ40 and Aβ42 in HEK293T cells

as compared to wt (2.5 to 10 fold). Levels of Aβ40 were significantly lower with only three

mutants: K699A, V710A and S697A/K699A (3.2, 2.6 and 3.5 fold less respectively). Cells expressing

the mutant E693K showed an increase of the number and size’s endosomes. Cholesterol-loaded

liposomes and non-mutated wt peptides corresponding to the CBS of APP showed a significant

interaction whereas mutant peptides did not.

These results suggest that a specific interaction between the CBS of APP and cholesterol

modulates the secretion of Aβ40 and Aβ42. Furthering our understanding of the interaction

between cholesterol and APP could reveal novel therapeutic strategies for the treatment of

sporadic AD.

Emily QUENTIN1, ImaneMoutkine1, Sabine Levi1, Philip Marin2, Luc Maroteaux1 - CIPP

scaffold protein: a new interactor ofC-terminal5-HT2B serotonergic receptor promote

signaling pathway activity 1U INSERM 839, 2IGF Montpellier

Serotonin receptor subtype 5-HT2B, a G-protein-coupled receptor, play an important role in

serotonergic signaling. It is already known that its activation can modulate the 5-HT

concentration by its action on serotonin transporter. In addition, 5-HT2B knock-out mice show a

lack of antidepressants effect of SSRIs, an impulsive behavior, a loss ofMDMA psychoactive

effects. Allthosedrugsaretargetingtheserotonin transporter, it is why is crucial to know the

molecular mechanisms that are potentially disturbed in these processes. The 5-HT2B

receptorisstrongly associated to different kind of protein by its PDZ motif localized at the end of

its C-terminal extremity. Here we focused on channel interacting PDZ protein CIPP, a multivalent

PDZ domain protein know to form proteins complex and could act as an important

modulatorofglutamatergic transmission by its association to NMDA receptors. The present

study using transiently transfected cos-7 cell, show that interactions between 5-HT2B serotonergic

receptor and CIPP significantly increase signaling pathway activation in basal and stimulated

conditions without affecting G protein coupling efficiency to the receptor. Also,

pharmacological binding experiments indicates that association doesn’t affect the total and

plasma membrane expression of 5-HT2B receptor. Trafficking experiments using transiently

transfected primary culture of hippocampal neurons allowed us to identify CIPP clustering of 5-

HT2B receptors and modulation of its subcellular distribution.

Emilie SIMONNET, SabrinaMartin-Pires,LucPardanaud,AnneEichmann and Isabelle

Brunet - RoleofEphrine-A4 in the development and in the physiology of arterial

innervation

Molecular Control of Neurovascular Development - Collège de France

Arteries receive a sympathetic innervation which is crucial to control their contraction level.

Arterial innervation (AI) settles from post-natal day 2 (P2) to adult in mice. Gene expression

comparaison of non-innervated (P0) and innervated (P2) arteries showed that EphrinA4, a

repulsive axon guidance molecule, is surprisingly expressed by arteries at the onset of

innervation. Therefore we aimed to assess the role of EphrinA4 signalisation in the development

and the physiology of AI in mice. We showed by immunostaining and in situ hybridization that

EphrinA4 is expressed by resistance arteries and identified EPHA4 as the EphrinA4 receptor

expressed by sympathetic neurons (SN). In vitro EphrinA4 binds to WT SN and induces their

collapse, but not on SN from EphA4-/- mice. As an anatomical consequence of a lack of axonal

repulsion, EphrinA4-/- and EphA4-/- mice exhibit an enhanced AI at P2 which remains in adult.

We inactivated specifically EPHA4 within SN using THCre-EphA4flox/flox mice and showed an

increased AI in ear skin and on oesophagus. As peripheric vascular resistance is involved in the

regulation of blood pressure (BP) we hypothetized that the defects in AI observed in our mice

could lead to hypertension. We are currently investigating this hypothesis using telemetry. We

also investigated AI of organs regulating BP using the 3DISCO technic to stain the whole heart

and kidney. Our preliminary results suggest that EphrinA4/EphA4 signalisation would be involved

in cardiac and renal SI, showing an increased and more spread innervation. In conclusion,

EphrinA4 is expressed by arterial smooth muscle cells and interacts with EphA4 to induce

collapse of SN in vitro. In vivo this can be associated with elimination of inapropriate or

outnumbered contacts between SN and arteries. As peripheric vascular resistance is involved in

the regulation of BP, understanding development and physiology of AI could help us to open

new therapeutic ways for hypertension.

Pathophysiology

Mathieu BUONAFINE, Dr B. Gravez, Dr E. Martinez Martinez, Pr F. Jaisser and Dr C.

Amador – Implication of the Neutrophil Gelatinase-Associated Lipocalin (NGAL) from

immune cells in aldosterone induced cardiovascular remodeling

INSERM - Unité 1138, Equipe 1 - Esc E, 1er étage (Paris, France)

Background: Inadequate activation of the Mineralocorticoid Receptor (MR) promotes

hypertension, inflammation and fibrosis. Neutrophil Gelatinase-Associated Lipocalin (NGAL), a

pro-inflammatory/fibrotic glycoprotein, is a direct target of the MR in cardiovascular cells, and is

increased in immune cells during inflammation. Recently, we demonstrated that NGAL is crucial

for the hypertensive and pro-fibrotic effects of the nephrectomy-aldosteronesalt (NAS)

challenge in mice. However, the specific cell types that modulate NGAL production during

aldosterone-dependent hypertension are still unknown. The aim of this study was to characterize

the implication of NGAL produced by immune cells in the pathophysiological effects of MR

activation by aldosterone.

Materials and methods: In vivo: Male C57Bl6 mice were submitted to 28 days of NAS challenge

(200μg/kg/d). Peripheral blood mononuclear cells (PBMC) were isolated, and CD4+, CD8+ T

cells, B cells, Dendritic cells (DCs) and Macrophages (Mø) were sorted from the animals’ spleen.

In vitro: DCs and Mø were cultured from WT and NGAL-KO mice and treated with aldosterone

(100nM) for 24h.

Results: In vivo: NAS mice presented high systolic blood pressure (123 mmHg vs. Sham 101±6

mmHg, p<0.05), and cardiac/renal hypertrophy. NGAL abundance was found higher in PBMCs,

DCs and Mø, and further increased in NAS mice. In vitro: MR activation by aldosterone in DCs

induced an upregulation of NGAL and cytokines involved in the adaptive immune response

(TGF-β1, IL-23). Interestingly, the absence of NGAL in DCs cultured from NGAL-KO mice

prevented this increase.

Conclusion: MR activation and subsequent NGAL induction in DCs could play a pivotal role in

the inflammation observed during aldo-dependent hypertension.

Olivier CLAUDE, Elisa YANIZ-GALENDE, Maguelonne ROUX, Claire PERRET, David-

Alexandre TREGOUET and Jean-Sébastien HULOT - Identification of selective adult

cardiac progenitor cells (CPCs) surface markers by proteogenomics approaches

UMRS1166 – UPMC/INSERM, 91Bvd de l’hôpital, 75013 PARIS.

The presence of adult stem cells within the myocardium has only been recently acknowledged.

Using a transgenic mouse model expressing the bgalactosidase under the control of the PW1

gene, a marker of adult stem cell in numerous tissues, we have been able to identify new

populations of CPCs that contribute to myocardial repair after infarction. PW1 is however a

nuclear factor thus prompting for the identification of novel cell surface markers.We aim to

describe the membranome of those CPCs and its modification after MI in order to characterize

the function of those cells and in order to facilitate future studies.CPCs were collected from PW1-

bGAL mice normal and ischemic (7 days post MI) hearts using FACS. We used filtered, aligned,

quality controlled RNA-seq output files from each CPC population and condition (normal vs.

ischemic hearts) and converted RNA sequences into predicted protein sequences

(~40000/condition). A bioinformatic pipeline has been implemented in a Galaxy server to make

lists of putative membrane proteins by predicting the presence of signal peptides targeting

proteins to the membrane (SignalP3.0, WoLFPSORT) and transmembrane domains (TMHMM2.0)

but without nuclear localization signal (NLStradamus, PredictNLS).By progressive filtering, we

generated a list of candidates expressed in CPCs’ membranes (~2000/condition). By comparing

these different sub-types of CPCs and conditions protein lists, we identified cell type-specific and

condition-insensitive cell surface markers (~100proteins). Several databases were then cross-

checked to discard false positive results and a homebrew script was designed to create a

specific peptide list including sequences and molecular weight for the ~70 selected proteins.

Using same cells collected from the FACS, we proceed to a membrane protein enrichment

using a biotin coupled reagent. Sample will then undergo common proteomic treatments

before an LC-MS run in which we seek the specific peptide list previously described.

Irma Karen LOPEZ CAYUQUEO, Régine Chambrey, Jacques Teulon, Francisco V.

Sepúlveda, Isabel Cornejo and L. Pablo Cid - Knockin of HA-tagged K+ channel Kir7.1

as a tool to determine its segmental and subcellular localisation in mouse kidney.

PARCC INSERM U970, Centro de Estudios Cientificos (CECs).

Kir7.1 is an inwardly rectifying K+ channel of the Kir superfamily encoded by the Kcnj13 gene. This

channel is present in epithelial tissues where it was found to colocalize with the Na+/K+ pump by

immunohistochemistry and it was thus suggested it could serve to recycle K+ taken up by the

pump. We generated a mouse lacking Kir7.1 by ablation of the Kcnj13 gene; the homozygous

mutant null mice die hours after birth and show cleft palate and moderate retardation in lung

development.

In order to study more precisely the localisation of the Kir7.1 channel in tissues, we created a

Kir7.1 HA-tagged knockin mouse by the CRISPR/Cas9 method. The HA epitope (YPYDVPDYA)

was inserted between residues 90 and 91 of the extracellular loop of Kir7.1 channel. Additionally

one glycine (G) was added at the N-terminus of the epitope in order to improve both the

mobility of the tag and antibody recognizing. The insertion did not alter the function of Kir7.1 as

demonstrated in electrophysiological experiments on the channel in a heterologous expression

system. Our results corroborate previous localisation of Kir7.1 in choroid plexus and retinal

pigment epithelium, where the channel is seen at the apical membrane of these epithelial cells.

In the kidney, Kir7.1 protein was found only in the papilla by immunoblot analyses of the HA tag

on lysates of cortex, outer medulla and inner medulla. This restricted localisation does not fit with

previous immunohistochemistry studies on guinea pig, rat and human kidneys, in which the use

antibodies against Kir7.1 showed expression of this channel in the basolateral membrane of

various tubular structures in both cortex and medulla. Until now there was no report on the

localisation of this channel in the mouse kidney. The Kir7.1 HA-tagged mouse therefore is a good

tool to decipher the role of this potassium channel in the renal papilla, where important

processes such as urine concentration take place.

Ahmad MASSARWEH1,2,4, Michaël Bosco3, Soria Iatmanen-Harbi1,2, Clarice Tessier1,2,

Nicolas Auberger3, Patricia Busca3, Isabelle Chantret1,2, Christine Gravier-Pelletier3 and

Stuart E. H. Moore1,2 - Golgi Dolichol linked Oligosaccharide (DLO) Diphosphatase, a

potential regulator of DLO metabolism 1INSERM U1149, Paris, France. 2Université Denis Diderot, Paris 7, Paris, France. 3Université Paris Descartes, CICB-Paris, CNRS UMR8601, LCBPT, 45 rue des Saints-Pères, 75006 Paris, France. 4Université Pierre et Marie Curie, Paris 6, Paris, France.

Background: Type I congenital disorders of glycosylation (CDG-I) are caused by genetic defects

in the Dolichol-Linked Oligosaccharide (DLO) biosynthetic pathway. These mutations result in the

accumulation of DLO intermediates and protein hypoglycosylation. Although protein

hypoglycosylation is thought to be the main pathogenic factor in CDG-I, the pathogenic effect

and fate of truncated DLO intermediates is not understood. Truncated DLO intermediates in

patient’s cells are known to give rise to cytosolic Oligosaccharyl Phosphates (OSP) by an

uncharacterized mechanism. To understand this DLO editing process; characterization of the

activity that generate OSP at the molecular and biochemical levels is needed.

Materials, methods and results: Using classical biochemical approaches we characterized a

Co2+ activated DLO diphosphatase which has a pH optimum 5.5 and generates OSP and

dolichyl phosphate from DLOs. Differential centrifugation of mouse liver showed a microsomal

localization of this activity. Fractionation of microsomes on self-forming density gradient

demonstrated that the activity doesn’t co-localize with the Endoplasmic Reticulum (ER)-situated

dolichol cycle enzymes (where DLOs are synthesized and utilized) but with the Golgi Apparatus

(GA)-situated marker (UGT). The unexpected localization profile prompted us to study OSP

generation in cells using Brefeldin A (BFA) which fuses elements of GA with ER. BFA caused a

striking increase in OSPs that have Golgi modified structures. Further OSP localization studies

using permeabilized cells revealed that BFA induced OSP generation in the lumen of the BFA

compartment contrary to cytosolic OSPs generated in CDG-I cells which was not affected by

BFA treatment.

Conclusion: OSP generation is a complex process governed by at least two mechanisms

depending on DLO structure, membrane orientation and localization. We propose that the GA

situated DLO diphosphatase may play a role in degrading the DLO that escape the ER.

Meriam NEFLA, Laure SUDRE, Guillaume DENAT,Sabrina Priam, Gwenaëlle Andre-Leroux,

Francis BERENBAUM and Claire JACQUES - The proinflammatory cytokine 14-3-3ε is a

ligand of CD13 in cartilage.

CDR Saint-Antoine UMR_S 938, 184 Rue du Faubourg Saint-Antoine, 75012 Paris

Background: Osteoarthritis (OA) is a whole-joint disease characterized by progressive destruction

of articular cartilage involving abnormal communication between subchondral bone and

cartilage. Our team identified 14-3-3ε protein as a subchondral bone soluble mediator altering

cartilage homeostasis. This protein acts as a potent stimulatory factor of MMP-3 and MMP-13

involved in the degradation of cartilage matrix in OA. CD13/APN, potential receptor of this

protein, was identified on the surface of chondrocytes. The aim of this study was to investigate its

involvement in chondrocytes response to 14-3-3ε.

Methods: CD13/APN was invalidated using siRNA or blocking antibodies in articular

chondrocytes. Chondrocyte expression and release of MMP-3 and MMP-13 were evaluated by

RT-PCR and ELISA. The aminopeptidase N (APN) activity was assessed in chondrocytes

supernatant using the fluorescent substrate L-alanine β-naphtilamide. The interaction between

14-3-3ε and CD13 was studied by surface plasmon resonance, biotinylation and in silico studies.

Results: mRNA expression and protein release of MMP-3/-13 induced by 14-3-3ε reduce

significantly after CD13/APN invalidation. APN activity was identified in chondrocytes. However,

it was unchanged following chondrocyte stimulation with 14-3-3ε. Direct interaction was showed

between recombinant CD13/APN and 14-3-3ε (78 RU). Using labeled 14-3-3ε, we also found that

14-3-3ε binds to the surface of chondrocytes in a CD13 dependant manner . Finally, we

identified EFNpYVW as the CD13 peptide sequence required for the recognition of 14-3-3ε.

Conclusions: These results suggest that CD13 plays its receptor role to bind 14-3-3ε and transmit

its signal in chondrocytes to induce a catabolic phenotype similar to that observed in OA. Thus,

14-3-3ε-CD13 interaction could be a novel therapeutic target in OA.

Benjamin VALLIN, Régis Blaise, Isabelle Limon - Identification of a new adenylyl cyclase

8 (AC8) isoform: implication in vascular smooth muscle cells (VSMCs)

transdifferentiation and pathological vascular remodeling

UMR 8256 Biological Adaptation and Ageing

Atherosclerotic lesion expansion and post-angioplasty restenosis result primarily from the

transdifferentiation of VSMCs into migratory/proliferative/inflammatory/secretory cells. Cyclic

AMP, whose production and degradation are catalyzed by adenylyl cyclases (AC) and

phosphodiesterases (PDE) respectively, plays a key role in modulating VSMCs phenotype

(Yokoyama, 2010).

We showed that the transdifferentiation of VSMCs into inflammatory/migratory cells in vitro

depends on de novo expression of the transmembrane AC isoform 8. The pathological VSMCs in

human atherosclerotic lesions have high AC8 levels. AC8 knockout in ApoE-/- mice decreased

aorta inflammation and lesion size; the siRNA-mediated knockdown of AC8 reduced neo-intima

formation in a rat model of postangioplasty restenosis.

We recently discovered that 90% of the AC8 in transdifferentiated (td) VSMCs consists of a newly

identified splice variant lacking the first five transmembrane domains: AC8D.

Immunocytochemistry and AC activity assays revealed a profound change in membrane

topology knocking AC8D activity. Surprisingly, studies with FRET-based biosensors showed that

AC8D limits cAMP accumulation within the cell. Studying cAMP synthesis over time, we showed

that AC8D has no effect on cellular AC activity. Thus, the inhibition of cAMP accumulation results

from an increase in PDE activity, suggesting a role for AC8D in physically recruiting PDE, by direct

activation or subcellular relocalization. Furthermore, using AC8D-specific siRNA, we

demonstrated the involvement of AC8D in the transdifferentiation of VSMCs into inflammatory

cells.

Increases in cellular cAMP inhibit the migratory (McKean, 2015), proliferative (Hewer, 2011) and

inflammatory (Aoki, 2010) properties of tdVSMCs. Thus, AC8D may participate in atherogenesis

and restenosis by maintaining the pathological phenotype of tdVSMCs. We are investigating the

mechanisms involved and trying to confirm the role of AC8D in pathological vessel remodeling.

ORAL COMMUNICATIONS - 26th May 2016

Immunology & Inflammation

Mélanie CRON, Frédérique Truffault, Ambra Vittoria Gualeni*, Annunziata Gloghini*,

Sonia Berrih-Aknin and Rozen Le Panse - Characterization of the role of miR-150 in

autoimmune Myasthenia Gravis

UPMC - UMRS 974 - INSERM - FRE 3617 CNRS - AIM Centre de Recherche en Myologie - Hôpital de La Pitie-

Salpétrière

*Department of Pathology and Laboratory Medicine, Istituto Nazionale dei Tumori, Milano, Italy

Myasthenia gravis (MG) is an invalidating disease mediated by autoantibodies against the

acetylcholine receptor at the neuromuscular junction and leading to muscle weaknesses. In

MG, the thymus is the effector organ and is often characterized by B-cell infiltrations leading to

ectopic germinal center (GC) development. MicroRNAs are small noncoding RNAs that regulate

protein expression through direct interactions with mRNAs. They are involved in many

physiological and pathophysiological processes, including autoimmune diseases. In

collaboration with a Swedish team, we demonstrated that miR-150 was upregulated in the

serum of MG patients, and was significantly downregulated after thymectomy in correlation with

disease improvement.

The aim of this study was to determine the potential role of miR-150 in MG patients by

investigating its expression in the thymus.

We showed that miR-150 was upregulated in the thymus of MG patients with numerous GCs. We

did not observe any miR-150 increase in thymic epithelial cells or in thymocytes from MG patients

compared to controls. However, miR-150 increase was correlated with thymic expression of the

B-cell marker CD19. By in situ hybridization, we demonstrated that miR-150 was strongly

expressed in naive B cells located in the mantle zone around GCs.

We also observed that thymic expression of c-Myb, a well-defined target of miR-150, was down-

regulated and inversely correlated with the expression of miR-150. In naïve B cells of the mantle

zone, miR-150 expression is probably involved in the regulation of c-Myb at a posttranscriptional

level, blocking B-cell differentiation.

Altogether, we demonstrated that the thymic up-regulation of miR-150 in MG is correlated with

the abnormal development of GCs in patients. We are now investigating why miR-150 is

increased in the serum of MG patients and if this circulating miR-150 has a functional role in the

disease.

Clément LEVIN1,2*, Charles Nuttens1,2*, Olivia Bonduelle1,2, Helene Perrin1,2, Bernard

Verrier3 and Béhazine Combadiere1,2 - Role of skin migratory antigen-presenting cells in

T follicular helper cell polarization after intradermal vaccination

*Both authors contributed equally to this work 1Sorbonne Universités, UPMC Univ Paris 06, Unité Mixte de Recherche de Santé (UMR S) CR7, Centre

d’Immunologie et de Maladies Infectieuses – Paris (Cimi-Paris), F-75013, Paris, France 2Institut National de Santé et de Recherche Médicale (INSERM) U1135, Cimi-Paris, F-75013, Paris, France 3Institut de Biologie et Chimie des Protéines, Centre National de la Recherche Scientifique, Université

Claude Bernard de Lyon, 69367 Lyon

Cedex 07, France

Background: The skin is recognized as a promising route of immunization as it contains

specialized APC subsets such as Langerhans cells (LCs) and other dermal dendritic cells (DCs).

Upon immunization, DCs in tissues sample antigens and migrate to draining lymph nodes (DLNs)

where they interact with naïve T cells to promote their differentiation and effector functions. In a

previous work we showed that intradermal (i.d) immunization of mice with HIV-p24 poly lactic

acid (PLA) nanoparticles induced robust humoral and cellular CD8+ T cells responses, which are

crucial against HIV disease.

As T follicular helper (TFH) cells play a pivotal role in germinal center formation and B cell help,

we questioned the role of skin and DLN APCs in the induction of TFH cells and antibody-secreting

B cells after i.d vaccination.

Methods: Ablation of the injection site and conditional depletion of langerin+ cells were used to

evaluate the role of skin migratory cells and langerin-expressing cells respectively in TFH cell

induction. Moreover, fluorescent antigen-coated nanoparticules (NPs) were used as a vaccine

model to enable tracking of NPs+ cells.

Results: We found that skin migratory DCs are necessary for induction of TFH and antigen-specific

antibody-secreting B cells. Tracking of injected p24-PLA NPs revealed the high ability of LCs and

Langerin+ dermal DCs to capture antigen in the skin and migrate to the T/B interface of DLNs.

Further depletion of Langerin+ cells resulted in partial abortion of TFH polarization and p24-

specific IgG and IgA-secreting B cells expansion after immunization.

Conclusions: Work is currently in progress to elucidate the mechanisms by which skin mig DCs

promote such responses after i.d vaccination. Our work unravels a crucial role for skin cells and

particularly LCs in the induction of humoral immunes responses and TFH cell polarization after i.d

vaccination. It will provide cues for better vaccine development against infectious diseases such

as HIV.

Anastasia MIKHAILOVA1, Robbiati V2, Lasserre R2, Pinaud L2,3, Alcover A2, Rey F1 and

Thoulouze MI1,2 - The role of Tuba protein in the dynamics of immune synapse formation 1Structural Virology Unit, Department of Virology, Institut Pasteur, Paris, France 2Lymphocyte Cell Biology Unit, Department of Immunology, Institut Pasteur, Paris, France 3Molecular Microbial Pathogenesis, Department of Cell Biology and Infection, Institut Pasteur, Paris, France

T lymphocytes commonly make contacts between each other and antigen presenting cells

(APCs). The formation and signal propagation in activating contacts, termed immunological

synapses (IS), strongly depend on the reorganization of the cell’s cytoskeleton and intracellular

trafficking. However, the exact molecular players responsible for these events still remain poorly

understood.

Tuba is a multidomain scaffolding protein that has a lipid-binding BAR domain and interacts with

N-WASP and Cdc42, molecules coordinating cell polarization at the IS. Upon Tuba knockdown

(KD), T cells displayed reduced ability to retract from contacts with a glass surface but formed

less stable and symmetric IS with APCs. Moreover, T cell receptor (TCR) displayed fragmented

accumulation pattern at the IS, which was accompanied by increased cell activation, reflected

by higher IL-2 production. However, the identity of the intracellular events connecting the

change in the nature of contacts with increased T cell activation still needs to be determined.

We performed live cell imaging to directly observe real time dynamics of IS formation in Tuba KD

and control cells. When dropped on glass coated with activating anti-TCR antibody, T cells

transfected with C-terminal domain of Tuba (mimics KD) displayed higher asymmetry at the

contact interphase but there was no observable difference in the speed of TCR signaling

microclusters. Although no differences were observed in calcium signaling in Tuba KD cells and

controls during contacts (both activating and non-activating) with B cells, Tuba KD cells

displayed slower migration speed and less displacement during the interaction with dendritic

cells confirming retarded retraction pattern seen on glass.

We conclude that there are no differences between Tuba KD and control cells in the early

events of the cell signaling downstream of the TCR. Thus, the increase in activation is due to

changes in the late phase of the T cell contact dynamics.

Emmanuel STEPHEN-VICTOR1,2,3, Srini V Kaveri1,2,3,5, Jean-Paul Latgé4, Vishukumar

Aimanianda4 and Jagadeesh Bayry1,2,3,5 - Cellwallα-(1,3)-glucanfrom Aspergillus

fumigatus induces PD-L1 expression on human dendritic cells that regulates Th1 and

regulatory T cell responses 1Institut National de la Santé et de la Recherche Médicale Unité 1138, Paris, F-75006, France 2Sorbonne Universités, UPMC Univ Paris 06, UMR S 1138, Paris, F-75006, France 3Centre de Recherche des Cordeliers, Equipe - Immunopathology and therapeutic immunointervention,

Paris, F-75006, France 4Unité des Aspergillus, Institut Pasteur, Paris, F-75015, France 5Université Paris Descartes, Sorbonne Paris Cité, UMR S 1138, Paris, F- 75006, France

Background: Aspergillus fumigatus is an opportunistic pathogen that causes invasive

aspergillosis, a fatal disease in immune-compromised individuals. Cell wall polysaccharides are

the key immunogenic components of A. fumigatus. α-(1,3)-glucan, an amorphous component

of A. fumigatus cell wall forms a major proportion among cell wall polysaccharides suggesting

that this polysaccharide has a critical role in modulating immune response. In the present study

we investigated the role of A. fumigatus derived α-(1,3)-glucan in mediating human DC

response and the ensuing T cell response.

Materials and Methods: Human dendritic cells (DCs) were derived from circulating monocytes.

DCs were treated with α-(1,3)-glucan and the extent of DC maturation and activation was

analyzed by flow cytometry. The ‘α-(1,3)-glucan-educated’ DCs were co-cultured with

autologous naïve CD4+ T cells to delineate the polarization of T cell responses by flow cytometry.

Cytokine production by DCs and T cells was analyzed by ELISA.

Results: α-(1,3)-glucan induced maturation of DCs and secretion of various immunoregulatory

cytokines. Of note, activation of innate cells was partially dependent on TLR2. Analysis of CD4+ T

cell polarization revealed that α-(1,3)-glucan-stimulated DCs induced CD4+ CD25+FoxP3+

regulatory T cell (Treg) generation that was in part dependent on programmed death-ligand 1

(PD-L1) expression on DCs. Importantly, blockade of PD-L1 on DCs enhanced IFN-γ secretion

suggesting that PD-L1 acts as negative regulator of α-(1,3)-glucan-mediated protective immune

responses. Taken together, these results demonstrate that α-(1,3)-glucan diversifies the immune

response to A. fumigatus by their distinct abilities to polarize specific CD4+ T cell responses.

Conclusion: A. fumigatus derived α-(1,3)-glucan is an immunomodulatory polysaccharide that

imprints regulatory features on DCs which suppresses Th1 response and mediates Treg

generation.

Virology

Iratxe DEL RIO, Jérôme Bouchet, Andrés Alcover - HIV-1 modulation of the T cell

activation molecular machinery

Lymphocyte Cell Biology, Inserm U1221, Institut Pasteur, Paris

The actin and microtubule cytoskeleton, together with polarized vesicle traffic, play a major role

in the formation and function of immunological synapses, ensuring the spatiotemporal

localization of the T cell receptor (TCR) and different signaling proteins. Our laboratory showed

that HIV-1 subverts the formation of immunological synapses. Indeed, HIV-1, through its protein

Nef, interrupts the intracellular transport of the tyrosine kinase Lck, a key element of the TCR

signal transduction cascade, to the immunological synapse, inducing its accumulation in an

intracellular vesicular compartment.

We utilized wild type or Nef-deficient HIV-1 virus strains, expression vectors encoding Nef or

various cellular proteins, and state of the art microscopy techniques to characterize this Nef-

induced endosomal compartment. Experiments performed both with Nef-expression or HIV-1

infection of the Jurkat T cell line show that Nef recruits active (phosphorylated) forms of several

key TCR signaling molecules, like the TCRz subunit, the tyrosine kinase ZAP70 and Vav1 to the Lck

compartment, where they strongly colocalize with Lck. Nef also recruits Rac1, an important

GTPase involved in actin remodeling, in a compartment, different that the one of Lck, where

Rac1 and Nef fully co-localize. Importantly, we showed the interaction between Nef and Rac1

by co-immunopecipitation experiments. Therefore, Nef could modulate, through this interaction,

the actin cytoskeleton dynamics.

We also observed that FIP3, a Rab11 effector protein, participates in this Nef-induced Lck

accumulation in endosomes, as FIP3 silencing by siRNA, disassembles the Lck compartment and

counteracts the effect of Nef on Lck endosomal accumulation. As a result, FIP3 silencing

provides an opportunity to perturb the Nef-induced endosomal compartment to investigate its

relevance in the physiology of infected T lymphocytes in order to modulate their activation

state, their survival capacity and to improve viral replication.

Olivier LUCAR1, 2, Bin Su3, Valérie Potard4, Assia Samri1, Christiane Moog3, Patrice Debré1,

Vincent Vieillard1 and ANRS CO15 ALT study group - New Family of Neutralizing

Antibodies in HIV Asymptomatic Long-Term Non-Progressors 1Sorbonne Universités, UPMC Univ Paris 06, INSERM U1135, CNRS ERL8255, Centre d’Immunologie et des

Maladies Infectieuses (CIMI-Paris), Paris, France; 2InnaVirVax SA, Evry, France, 3INSERM UMR S-1109, Centre de Recherche en Immunologie et Hématologie, Faculté de Médecine,

Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Strasbourg,

France; 4Sorbonne Universités, UPMC Univ Paris 06, INSERM UMR-S 1136, Institut Pierre Louis d'Epidémiologie et de

Santé Publique, Paris, France

One of the most debated issues in HIV is: do Neutralizing Antibodies (NAbs) plays a protective

role during HIV infection?

Through a large series of studies, our team previously characterized the pathogenic effect of the

highly conserved 3S epitope of gp41 during HIV infection. By analyzing the immune response

induced in asymptomatic long-term non-progressor (ALT) patients, we recently observed that

25% patients elicited efficient neutralizing responses directed against a point-mutated form of 3S

(W614A-3S). Thus, we extensively characterized the neutralizing profile of this new family of Nabs.

Abs binding to 3S-WT (wild-type) or W614A-3S mutants were isolated from the sera of ALT

patients. Abs were purified from heat-inactivated plasma of ALT patients by

immunoprecipitation with synthetic W614A-3S peptides immobilized onto an amine-reactive

agarose support, concentrated with Centicon filter, and dialyzed against PBS. The functional

inhibitory profile of these Abs was defined using the well-standardized TZM-bl neutralization

assay, the neutralization assay on PBMCs, or the Fc-mediated inhibitory assay on macrophages.

We found that the anti-W614A-3S purified Abs display efficient and broad neutralizing activity.

They inhibit transmitted founder Tier 2 viruses, neutralize primary isolates on primary cells and

display Fc-mediated inhibitory functions at low concentrations. The detection of anti-W614A-3S

Abs was specifically correlated both with lower viral DNA (p<0.0001), viral load (p<0.0001), and

more functional CD4+ cells; suggesting that anti-W614A-3S neutralizing Abs participate in the

control of HIV replication.

These results demonstrate ALT patients develop efficient neutralizing Abs distinct of those

recently isolated from ELITE neutralizer patients. Abs directed against W614A-3S may therefore

be considered as a new family of broadly neutralizing Abs, which need to be further

characterized, considering their potential role on viral load and viral DNA.

Angeline ROUERS, Brunet H., Moris A., Graff-Dubois S. and collaborators - Follicular

helperT cells (Tfh) and memory B cell response during HIV-1 infection Center for Immunology and Microbial Infections (CIMI-Paris), INSERM U1135, CNRS ERL8255, UPMC UMRS

CR7 - Hôpital Pitie-Salpêtière – France

T follicular helper cells (Tfh) support multiple steps of B cell maturation and antibody production.

HIV infection is associated with a defect of Tfh in providing B cell help in vitro. Mechanisms

underlying these Tfh dysfunctions are not fully defined. However, few HIV-infected individuals

known as elite controllers (EC) are able to produce polyfunctional antibodies (Ab), which might

contribute to HIV control. We first studied Tfh cells in chronically HIV-infected patients and in a

second complementary approach, we explored B cell memory responses in EC.

We identified Tfh, germinal center Tfh and regulatory Tfh in HIV+ and HIV spleens by FACS. These

three populations were increased in HIV+ spleen as compared to HIV- spleens. Using cell sorting

combined with RT-qPCR, we reported a reduced mRNA expression of co-stimulatory, regulatory

and signal transduction molecules in HIV+ spleens. We also evidenced compromised

productions of IL-4 and IL-10 by splenocytes from HIV+ donors. In parallel, we noticed an

impaired maturation of B cells in HIV+ spleens.

In a cohort study, we compared memory B cell responses in the blood of EC, treated HIV+

patients and healthy controls. Based on CD27 and CD21 expression, we identified activated,

resting, tissue-like and intermediate memory B cell by FACS. Our preliminary analysis suggests

that a HLAB* 57neg subgroup of EC presents an altered differentiation of B cells as compared to

others. Using B cell Elispot assays, we determined frequency, IgG isotype and specificity of anti-

HIV memory B cells. In contrast to anti-HIV IgG2 and IgG3 secreting B cells, most EC exhibit a high

frequency of anti-HIV IgG1 secreting B cells.

My work highlights a defective Tfh differentiation, which might explain why B cell maturation is

severely affected in HIV-progressors. The status of HIV-controllers seems associated with the

presence of an IgG1 B cell memory response. Further work will highlight whether Tfh functions are

preserved in EC.

Zineb SBIHI1, Dossier A1,4, Galicier L3, Boutboul D3, Emarre A1, Parizot C1,2, B Hoareau5,

Abgalika F3, Autran B1,2, Oksenhendler E3 and Carcelain G1,2 - iNKT and Memory B cells

deficiency in HHV-8 Multicentric Castleman Disease. 1Sorbonne Universités, UPMC Univ Paris 06, Inserm, Centre d'Immunologie et des Maladies Infectieuses

(Cimi-Paris), UMR 1135, ERL CNRS 8255, 91 Boulevard de l'Hôpital, F-75013 Paris, France 2Sorbonne Universités, UPMC Univ Paris 06, Inserm, Centre d'Immunologie et des Maladies Infectieuses

(Cimi-Paris), UMR 1135, ERL CNRS 8255, 91 Boulevard de l'Hôpital, F-75013 Paris, Département

d’Immunologie, CHU Pitie-Salpêtrière, Assistance Publique-Hôpitaux de Paris, 47-83 bd de l'hôpital, F-75013

Paris, France 3Hôpital Saint-Louis, Immunologie clinique, F-75010 Paris, France 4Hôpital Bichat, Médecine Interne, F-75018 Paris, France 5Sorbonne Universités, UPMC Univ Paris 06, UMS30-LUMIC, Platerforme CyPS, Paris, France.

Human Herpes Virus-8 (HHV-8) related Multicentric Castleman Disease (HHV-8 MCD) is a

lifethreatening virally induced B cell lymphoproliferative disorder. CD1d-restricted invariant

Natural Killer T (iNKT) cells, are innatelike T cells, playing a key role in antiviral immunity in

particular in the control of Epstein Barr Virus (EBV) infected B cells. We analyzed iNKT cells in

blood and spleen samples from 32 HHV-8 MCD patients and showed that iNKT cell frequencies

were dramatically decreased. Moreover, iNKT cells of HHV-8 MCD patients displayed a

significant proliferative defect after stimulation with α-GalCer. This defective iNKT cell was

associated with altered B cell subsets distribution, with a significant decrease in memory B cells

far more pronounced in Marginal Zone B cells. However, we observed no defect in CD1d

expression in antigen presenting cells but we showed that the iNKT defects contribute to the B

cell subsets alteration. This study identifies for the first time a defect in iNKT cell in HHV-8 MCD

patients associated to an imbalance in B cell subsets. These observations may contribute to the

understanding of the complexe interaction between HHV-8 and immune system cells leading to

the development of HHV-8 related B cell malignancies in HHV-8 MCD patients.

Metabolism & Nutrition

Mengyue HU Franck PHAN, Isabelle HAINAULT, Fawaz ALZAID, Nicolas VENTECLEF, Olivier

BOURRON, Fabienne FOUFELLE - The role of receptor activator of NF-kB (RANK) and its

ligand (RANKL) in the Non-Alcoholic Fatty Liver Disease (NAFLD)

INSERM UMRS 1138, Centre de Recherches des Cordeliers, 75006 Paris, France

Background and aim: Chronic inflammation in liver plays an important role in the development

of non-alcoholic fatty liver disease (NAFLD), a metabolic syndrome that encompasses a

spectrum of diseases. The activation of Nuclear factor-kB (NF-kB) in liver contributes to steatosis,

insulin resistance, hepatic inflammation leading to hepatic fibrosis. Among the numerous system

that activates NF-kB, RANKL and its cognate receptor RANK have been recently reported to be

involved in the progression of insulin resistance and other metabolic diseases. The aim of the

project is to study the RANK/RANKL/NF-kB pathway in the onset and progression of NAFLD.

Methods: The expression of RANK and RANKL under different pathological conditions related to

NAFLD were measured in different cells of the liver (hepatocytes, Kupffer cells, and Hepatic

Stellate cells) and adipose tissue. To activate the RANK/RANKL pathway in vivo, recombinant

RANKL was injected for 4 consecutive days in wild type mice.

Results: Under NAFLD conditions, the expression of RANK and RANKL was induced in

hepatocytes, kupffer cells, and hepatic stellate cells, and the increase was more remarkable as

the inflammatory states aggravated. RANK and RANKL expression were also induced in the

adipose tissue of ob/ob mice, and adipocytes of diabetic patients.

After repeated injections of RANKL, no obvious alterations were observed in liver, but in

epididymal adipose tissue, numerous lipogenesis genes were induced, along with the induction

of proinflammatory cytokines. Similar increase of lipogenesis genes was also observed in

subcutaneous adipose tissue.

Conclusion: The expression of RANK and RANKL are increased in liver and adipose tissue under

conditions related to NAFLD. The activation of RANK/RANKL pathway could play a role in the

lipid metabolism of adipose tissue.

Cécilia LANDMAN, M. Clément, H. Nsiri, E. Quévrain, T. Bazin, L. Brot, J.-P. Grill, M.-A.

Maubert, L. Humbert, H. Sokol, G. Trugnan, D. Rainteau and P. Seksik – The N-acyl-

homoserine lactone 3-oxo-C12, an inter-bacterial signaling molecule (involved in

quorum sensing), exerts effects on the host: thus implicating quorum sensing in

Inflammatory Bowel Disease

UPMC, ERL INSERM 1157 / UMR7203, Paris, France

Background: Inflammatory bowel disease (IBD) associated dysbiosis causes profound changes in

gut microbiota. We have shown previously that the profile of inter-bacterial signaling molecules,

the N-acyl-homoserine lactones (AHLs), is altered during dysbiosis. In particular, we observed

deficiency in 3-oxo-C12:2, the dominant intestinal ecosystem AHL. The aim of this study was to

explore the ability of 3-oxo-C12, a structurally close AHL, to interact with eukaryotic intestinal

epithelial cells.

Methods: Firstly, the subcellular localization of fluorescently labeled 3-oxo-C12 was visualized, in

a human epithelial cell (Caco-2) model, by confocal microscopy. Additional staining included:

membranes stained with Lectin Wheat Germ agglutinin (WGA), nucleus with DRAQ 5 and

euchromatin with anti-histone3 antibody. Following this, we examined the effect of 3-oxo-C12 on

inflammation pathways. Experiments were carried out under a range of conditions including:

increasing concentrations in DMSO, with/without the paraoxanase (PON) inhibitor, 2-

hydroxyquinoline (2HQ) and with/without IL1β stimulation. Response was quantified by

measurement of IL-8 (ELISA) in the supernatant 18 hours post exposure to AHL.

Results: Confocal microscopy showed intracellular localization of 3-oxo-C12 (1μM) after 1 hour.

More specifically, we observed co-localisation with euchromatin suggesting a transcriptional

factor role for 3-oxo-C12 within the host cell.

When examining the effect of 3-oxo-C12 on inflammation pathways we observed a significant

decrease in IL-8 18 hours post stimulation with IL1β, in the presence of both 3-oxo-C12 (1 and

5μM) and 2HQ.

Conclusion: We have demonstrated that 3-oxo-C12, an AHL structurally close to 3-oxo-C12:2,

present in the human intestinal ecosystem interacts with eukaryotic cells by penetration of

intestinal epithelial cells. Additionally, 3-oxo-C12 exerts an anti-inflammatory effect, at low

concentrations, in the presence of PON inhibitors in the same cell model.

Ludovica MARINELLI1, Camille Martin-Gallausiaux1, Fabienne Beguet-Crespel1, Karine

Clément2, Hervé M. Blottiere1,3, Nicolas Lapaque1 - Activation of the AhR signal pathway

by the gut microbiota. 1Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay, Jouy-en-Josas, France; 2Institute of Cardiometabolism and Nutrition, ICAN, Assistance Publique Hôpitaux deParis, Pitie-Salpêtrière

hospital, Paris ; 3MGP MetaGenoPolis, INRA, Université Paris-Saclay, Jouy en Josas, France.

Microbiota shapes the host metabolic and immune network producing metabolites acting as

physiological or immunological modulators. Within these bacterial products, indoles have been

described as AhR ligand inducing anti-inflammatory response. However, the interplay between

host and microbiota is highly complex and the precise mechanism for microbial AhR stimulation

is still unclear. We aim to identify: i) the bacteria able to activate AhR, ii) the genes involved, iii)

the produced molecules and iv) the potential effect for the host. For this purpose, we screened

a collection of bacterial species on HT-29 cell line expressing an AhR luciferase reporter system

and we identified 32 AhR-activators and 15 AhR-inhibitors strains. Principal component analysis

evidenced a correlation between AhR activation and butyrate production that we confirmed

with pure butyrate. Test of other SCFA evidenced also a reproductive AhR activation by

propionate, isovalerate and valerate. To identify the mechanism by which butyrate activates

AhR, we tested the impact of agonists of G-protein coupled receptors (GPR) and inhibitors of

histone deacetylase (HDACi) on AhR activation. GPR agonists as well as HDACi did not mimic

the effects of butyrate, suggesting a mechanism independent of both GPR and HDAC. We test

therefore two AhR antagonists and we showed that both failed to completely suppress the

butyrate-induced response suggesting two different hypotheses: i) butyrate is not an AhR ligand;

ii) butyrate is an AhR ligand with mechanism of activation or affinity different from the known

ligands. We are currently studying the mechanism by which butyrate activates AhR, by

analysing the expression of some crucial partners of the AhR activation pathway. Interestingly

we also identified bacterial strains able to activate AhR without butyrate and propionate

production and these will be used to generate genomic libraries for the identification of the

bacterial metabolites and genes involved.

Hedi SOUSSI, Sophie Reggio, Rohia Allili, Cecilia Prado, Maria Pini, Christine Rouault,

Karine Clément and Isabelle Dugail - DAPK2 down-regulation associates with

attenuated adipocyte autophagic clearance in human obesity

INSERM U1166 – Nutrition and obesity – Systemic approaches University Pierre and Marie Curie, Paris, France

Obesity is defined by excessive accumulation of fat and represents a condition wherein the

proper sensing of nutrients and energy status present significant challenges at the cellular and

systemic levels. The subsequent emergence of metabolic alterations and oxidative stress lead to

inflammation and organelle dysfunction. In this context, the autophagy pathway, which

orchestrates the degradation of damaged cytosolic constituents, is expected to be a critical

process for metabolic adaptation and cellular homeostasis. We analyzed autophagic flux in

adipocytes from obese patients (undergoing bariatric surgery) and obese mice. Adenoviral

approaches were used in adipocyte cell line to modulate autophagy-related protein

expression.

We observed a downregulation of autophagy in adipocytes from obese patients and obese

mice. Moreover, the degree of fat cell hypertrophy is inversely associated to autophagy activity,

suggesting a link with lipid storage. Our transcriptomic analysis of obese adipose tissue showed a

strong downregulation of the gene coding death associated protein kinase 2 (DAPK2).

Interestingly, suppression of DAPK2 in vitro resulted in defective autophagy, whereas

overexpression of this kinase increased autophagy in adipocyte cell line. Finally we observed a

partial restoration of autophagic activity and DAPK2 expression in adipocyte after weight loss

induced by bariatric surgery.

These data showed a link between DAPK2 downregulation and defective autophagy in obesity

and suggest an involvement of this kinase in adipocyte dysfunction.

POSTERS

Wednesday, 25th May 2016 – 10:30 to 11:45

[1] ANDROUIN Alexandre, Youssef, I., Delatour, B. and Marty, S. - Endoplasmic reticulum stress

and neurodegeneration in a mouse model of Alzheimer's Disease

Team "Alzheimer's and Prions's diseases", Brain and Spinal cord Institute, Inserm U1127/CNRS UMR

7225/UPMC Univ Paris 06 UMR S 1127, Paris, France

[2] BEGUIER Fanny, Michael Housset, Sophie Lavalette, Sébastien Augustin, Xavier Guillonneau

and Florian Sennlaub - HTRA1 and subretinal inflammation in the context of Age Macular

Degeneration

Institut de la Vision U968

[3] BENABOU Eva, Corina Buta, Dominique Wendum, Olivier Scatton, Olivier Rosmorduc,

Françoise Praz, Laëtitia Fartoux and Christèle Desbois-Mouthon - Insulin receptor isoform A in

hepatocellular carcinoma

CdR Saint Antoine, UMR_S938

[4] BOTTE Alexandra, Jeanne Lainé (1), Gaëlle Fontaine (1), Agathe Franck (1), Dean Nizetic (2),

Orestis Faklaris (3) and Marie-Claude Potier (1) - Early endosomes agregation in Down Syndrome

and Alzheimer's disease (1) Institut du Cerveau et de la Moelle épinière, Paris

(2) Barts and London School of Medicine, Queen Mary University, London

(3) Plateforme ImagoSeine, Institut Jacques Monod, Paris

[5] BOUGACHA Nadia - Role of REL in drug resistance in Chronic Lymphocytic Leukemia

Centre de Recherche des Cordeliers UMRS 1138

[6] BOUVET Delphine (1,2), MUNIER Annie (3), SVRCEK Magali (1,2,4), DUVAL Alex (1,2) and

MULERIS Martine (1,2) - Diagnosis of Lynch syndrome: functional characterization of variants of

uncertain significance in mismatch repair genes

(1) INSERM UMRS 938 -Centre de Recherche Saint-Antoine, Equipe "Instabilité des Microsatellites et

Cancers", Paris, France

(2) Université Pierre et Marie Curie-Paris6, Paris, France

(3) UMS30-LUMIC, Plateforme de Cytométrie en Flux CISA, Université Pierre et Marie Curie, Paris, France

(4) AP-HP, Hôpital Saint-Antoine, Service d'Anatomie et Cytologie Pathologiques, Paris, France.

[7] BOUYGUES Anaïs, Paul Mésange, Sandrine Thouroude, and Annette K. Larsen - VEGF-directed

therapies directly attenuate the migration and invasion of colorectal cancer cells

Laboratory of Cancer Biology and Therapeutics, Centre de Recherche Saint-Antoine, Paris 75571, France;

Institut National de la Santé et de la Recherche Médicale U938, Paris, France; Université Pierre et Marie

Curie, Paris France.

[8] COHEN Romain (1), Elisabeth Hain (1), Olivier Buhard (1), Sylvie Dumont (1), Thierry André (1,

2), Magali Svrcek (1, 3), Alex Duval (1) - Molecular and clinical characterization of metastatic

colorectal cancer with microsatellite instability

(1) INSERM, Unité Mixte de Recherche Scientifique 938, Centre de Recherche Saint-Antoine, Equipe B

Instabilité des Microsatellites et Cancers, Equipe labellisée par la Ligue Nationale contre le Cancer, 184 rue

du Faubourg Saint-Antoine, Paris 75012, France

(2) Department of Medical Oncology, Hospital Saint-Antoine, APHP, 184 rue du Faubourg Saint-Antoine,

Paris 75012, France

(3) Department of Pathology, Hospital Saint-Antoine, APHP, 184 rue du Faubourg Saint-Antoine, Paris 75012,

France

[9] DEZAIRE Ambre1,2, Nathalie Ferrand1, Marine Vallet2, Michèle Sabbah1, Anette K. Larsen1,

Soizic Prado2, Alexandre Escargueil1 - Characterization of bioactive molecules derived from

marine microorganisms, interfering with cell dedifferentiation processes observed at the invasive

front of mammary tumors 1INSERM UMR_S 938 Hôpital Saint Antoine Bâtiment Kourilsky 184, rue du Faubourg St Antoine 75571 Paris

Cedex 12 2UMR 7245, MCAM, CNRS, Muséum National d’Histoire Naturelle, 63 Rue Buffon, 75005 Paris, France.

[10] GEORGE Caroline, Martin Holzenberger and Saba Aïd - Suppression of Neuronal IGF

Signaling Protects from Proteotoxicity and Regulates Cell Size-controlling Pathways

INSERM, Centre de Recherche UMR938, Hôpital Saint-Antoine, and Sorbonne Universités, UPMC - Université

Pierre et Marie Curie, 75012 Paris, France.

[11] GOFAS SALAS Elena (1,2) , M. Pâques(2), C. Petit(1) and S. Meimon (1) - Paris’s High Speed

Adaptive Optics Flood Illumination Ophtalmoscope

(1) ONERA, The French Aerospace Lab, Châtillon, France

(2) CIC 1423, INSERM, Quinze-Vingts Hospital, Paris, France

[12] GREENE Malorie, Ada COLLURA, Alex DUVAL - Consequences of Coding Microsatellite

Instability in Colorectal Cancer: The balance between Transformators and Survivors genes. INSERM, U938

[13] HIRSCH Pierre, TANG, R., FAVA, F., MARZAC, C., DOUAY, L. and DELHOMMEAU, F. - A

phylogenetic strategy for minimal residual disease evaluation in acute myeloid leukemia

AP-HP Hôpital Saint-Antoine, CDR Saint-Antoine

[14] HUR Justine*, Claire KANONY-TRUC #, Thierry CLERC #, Isabelle LIMON* and Régis BLAISE -

Effects of omega-3 fatty acid on cerebrovascular alterations and inflammation in Alzheimer's

disease.

* UMR 8256 Biological Adaptation and Ageing, Université Pierre et Marie Curie, 7 quai Saint Bernard, 75252

Paris, France

# Institut de Recherche Pierre Fabre, 3 avenue Hubert Curien, 31035 Toulouse, France.

[15] LAVIGNE Jeremy, Valérie Buard, Frédéric Soysouvanh, Fabien Milliat and Agnès François -

Consequences of total or endothelial-specific PAI-1 deletion on radiationinduced lung damage

in mice. Institute for Radiological Protection and Nuclear Safety, Fontenay-aux-Roses, France

[16] LIU Jin - The influence of Neurotensin/Neurotensin receptor 1 complex on chemotherapy in

ovarian cancer

INSERM UMR-S 1007

[17] LIU Yuanhui - Role of Small ArfGAP-1 (SMAP1), an Arf6-specific GAP, on EGFR signaling upon

stimulation with various EGFR ligands in the Hep3B hepatocellular carcinoma human cell line

INSERM U938

[18] LOBE Cindy, Vaquero, J., Aoudjehane, L. and Fouassier, L. - Function of cancer-associated

fibroblasts in therapeutic sensitivity to anti-EGFR in cholangiocarcinoma

INSERM, UPMC, La Ligue contre le Cancer

[19] LOISEAU Camille and Laurence Bodineau - Enhancement of the respiratory response to

metabolic acidosis in newborn rat by a progestin. Possible involvement of orexin neurons.

UMR_S 1158 UPMC Neurophysiologie Respiratoire Expérimentale et Clinique - 91 Boulevard de l'Hôpital

Faculté de Médecine de l'Université Pierre et Marie Curie - Site Pitié Salpêtrière

[20] MAREK Veronika*, K. Kessal*, E. Reboussin*, L. Riancho*, G. Rabut**, A. Reaux-Le Goazigo*,

A-L. Raveau*, S. Melik-Parsadaniantz*, C. Baudouin **, T. Villette*** and A. Denoyer** - Clinical,

cell and genomic investigation of the role of light in the dry eye disease

* Paris Vision Institute, UMRS 968 (INSERM, UPMC University of Paris, CNRS), Paris, France

** Quinze-Vingts National Ophthalmology Hospital, Paris, France

*** Essilor International, R&D Department, Paris, France

[21] MEJECASE Cécile1, Caroline Laurent-Coriat2, Saddek Mohand-Saïd1,2, Aline Antonio1,2, Fiona

Boyard1, Christel Condroyer1, Steven Blanchard3, Mélanie Letexier3, Jean-Paul Saraiva3, Jose-

Alain Sahel1,2,4,5,6, Isabelle Audo1,2,4,5* and Christina Zeitz1* - Identification of a novel homozygous

mutation confirms the implication of GNAT1 in rod-cone dystrophy 1Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Institut de la Vision, 17 rue Moreau, 75012 Paris,

France. 2CHNO des Quinze-Vingts, DHU Sight Restore, INSERM-DHOS CIC1423, 28 rue de Charenton, 75012 Paris,

France. 3IntegraGen SA, Genopole, CAMPUS, 1 bat G8 FR-91030 EVRY, Paris, France 4Institute of Ophtalmology, University College of London, London, United Kingdom. 5Fondation Ophtalmologique Adolphe de Rothschild, Paris, France. 6Academie des Sciences, Institut de France, Paris, France.

*These authors contributed equally to this work, both are corresponding authors

[22] PECKEU Laurène1, Véronique Sazdovitch3, Nicolas Privat1, Arlette Welaratne2, Jean-Louis

Laplanche4, Danielle Seilhean3, Armand Perret-Liaudet5, Jean-Philippe Brandel1,2 and Stéphane

Haïk1,2,3 - Iatrogenic CJD after human GH treatment in France: effect of sex, dose and genetics

on the susceptibility of a possible infection by a V2 sCJD strain 1Institut du cerveau et de la moelle épinière (ICM) - Team "Alzheimer's

and Prion diseases"Inserm UMR-1127/CNRS UMR 7225, Université Pierre & Marie Curie - Paris 6 2AP-HP, Cellule Nationale de Référence des maladies de Creutzfeldt-Jakob, Groupe Hospitalier Pitie-

Salpêtrière, Paris, France 3AP-HP, Laboratoire de Neuropathologie R Escourolle, Groupe Hospitalier Pitie-Salpêtrière, Paris, France 4UF de Génétique Moléulaire, pôle B2P, Hôpital Lariboisière, Paris, France 5Hospices Civils de Lyon–Laboratoire Diagnostic Maladies à Prions; CNRS, Inserm, UCB Lyon1, Centre de

Recherche en Neurosciences de Lyon, BioRan, Bron, France.

[23] PHAM Thi Minh Tam1, Mona Munteanu1,2, Yen Ngo2, An Ngo2, Valentina Peta1,2, Luckina

Elena3, Djamel Elaribi3, Muriel Legroux3, Noemi Seurat3, Léa Verglas3, Thierry Poynard1,3 and Olivier

Lucidarme3 - Evaluation of combination ultrasound, shear wave elastography, and serum

biomarkers in the ultra-early diagnosis of hepatocellular carcinoma 1University Pierre Marie Curie, UMR_S 938, Research Centre Saint-Antoine; 2Research Unit, Biopredictive, Paris, France; 3Groupe hospitalier Pitie-Salpêtrière.

[24] SIQUEIROS Lourdes1,3, Hugo Charles-Messance1, Rodrigo Bolaños-Jimenez4,5, Cecilia

Montañez3, José Alain Sahel1,2, Alvaro Rendon1, Ramin Tadayoni1,6, Audrey Giocanti-Aurégan7 -

Role of Dexamethasone preventing Müller glial cells swelling. 1Institut de la Vision/INSERM/UPMC Univ Paris 06/CNRS/CHNO des Quinze-vingts, Paris, France. 2Fondation Ophtalmologique Adolphe de Rothschild, Paris, France. 3Genetics and Molecular Biology Dept, CINVESTAV, Zacatenco unit, México City. 4Association to prevent blindness in Mexico, Dr. Luis Sanchez Bulnes Hospital, México City. 5Ophthalmology Department, Regional Hospital, Adolfo López Mateos, ISSSTE, México City 6Ophthalmology Dept, Hôpital Lariboisière, AP-HP, Univ Paris Diderot, Paris, France. 7Ophthalmology Dept, Avicenne hospital, 125 rue de Stalingrad 93000 Bobigny.

[25] SOYSOUVANH Fréderic and Milliat Fabien - Endothelial senescence induced by radiation

and effects on healthy tissues

Institut de Radioprotection et de Sûreté Nucléaire (IRSN).

[26] VAN EEGHER Sandy, Maria-Luisa Perez-Lozano, Danièle Citadelle, Audrey Pigenet, Francis

Berenbaum and Xavier Houard - Consequences of hypertrophic chondrocyte differentiation on

osteochondral angiogenesis in osteoarthritis

INSERM UMR-S 938, UPMC, Saint Antoine research center, F-75571 Cedex 12, Paris, France.

Department of Rheumatology and “Inflammation-Immunopathology-Biotherapy” (DHU i2B), AP-HP Saint-

Antoine Hospital, F-75012 Paris, France.

POSTERS

Wednesday, 25th May 2016 – 15:30 to 16:45

[27] BATAILLE Aurélien2, P. Galichon2, N. Chelghoum1, B. Mohand-Oumoussa1, MJ. Ziliotis2, I. Sadia2,

N. Simon2, D. Legouis2, E. Rondeau2 and A. Hertig2 - Acceleration of renal fibrogenesis following

acute kidney injury: insights from the transcriptome of proximal tubules isolated ex vivo 1Plate-forme P3S, Faculté de Médecine Pierre & Marie-Curie, Paris, France 2Inserm UMR_S 1155, Paris, France

[28] BAUM David Marcel1, M Saussereau1, F Jeton2, N Voituron2, C Planès2, P Cardot1, L Bodineau1,

MN Fiamma1 - Obstructive sleep apnea – affecting serotonin signaling without affecting serotonin? 1UMR_S1158 Inserm-Université Pierre et Marie Curie - Neurophysiologie Respiratoire Expérimentale et Clinique -

Physiologie et Plasticité du Contrôle Respiratoire, Faculté de Médecine Pierre et Marie Curie site Pitie-

Salpêtrière - 91 Boulevard de l'Hôpital - 75634 Paris cedex 13, France 2Laboratoire HYPOXIE & POUMON - EA2363 - Université Paris 13, Sorbonne Paris Cite - 74 rue Marcel Cachin -

93017 BOBIGNY Cedex, France.

[29] BEURIOT Adeline, Catherine Eichel, Florent Louault, Alain Coulombe, Stéphane Hatem and Elise

Balse - Involvement of CASK protein domains in the down regulation of the sodium channel Nav 1.5

in cardiomyocytes INSERM UMRS_1166, Université Pierre et Marie Curie, Paris, France

[30] BOITARD Solène, Pierre Joanne, Maria Kitsara, Hany Naemetalla, Valérie Vanneaux, Mathieu

Pernot, Jérôme Larghero, Patricia Forest, Yong Chen, Philippe Menasché and Onnik Agbulut -

Nanofibrous Clinical-grade Collagen Scaffolds Seeded With Human Cardiomyocytes Induces

Cardiac Remodeling In Dilated Cardiomyopathy

University Pierre et Marie Curie, Paris Descartes, Ecole Normale Supérieure, Saint-Louis Hospital, BioM'up

industry, Georges Pompidou European Hospital, Langevin institut.

[31] CAMPION Sébastien, X. Navarro , M. Chavez, P. Pouget, T. Similowski* and M. Raux - Respiratory

discomfort assessment with visual evoked potentials.

INSERM UMR_S 1158 : CAMPION, SIMILOSWKI, RAUX

INSERM UMR_S 975 : NAVARRO, CHAVEZ, POUGET

Département d'Anesthesie-Réanimation, GHPS : RAUX

Pneumologie et Réanimation Médicale, GHPS : SIMILOWSKI

[32] DAHER Marie-Thérèse (1), Raphael Riclet (2), Olivier Rohr (2), Pedro Bausero (1), Pentao Liu (3),

Zhenlin Li (1) and Ara Parlakian (1) - Bcl11b, a transcriptional repressor: Its Role in cardiac

homeostasis and hypertrophy

(1) IBPS, Biological Adaptation and Ageing, UMR 8256, CNRS, INSERM U1164, Université Pierre et Marie Curie,

PARIS, FRANCE

(2) Université de Strasbourg, Strasbourg, FRANCE

(3) Wellcome Trust Institute, Cambridge, UK

[33] DELOUX Robin and Mathias Mericksay - Role of NAD/Nmrk2 signaling pathway in exercise

response during ageing

UPMC

[34] DESBOIS Anne-Claire, M Garrido, A Leroyer, J Gaudric, C Comarmond, D Klatzmann, P Fourret,

L Chiche, F Koskas, G Kaplanski, P Cacoub and D Saadoun - Interleukin 33 in large vessels

vasculitis.

IINSERM UMR_S 959 I3

[35] ESCRIBANO VAZQUEZ Unai and CHERBUY Claire - The role of a commensal Escherichia coli in

the interactions within microbiota-intestinal epithelium

INRA

[36] HAMMOUDI Nadjib, Alexandre Ceccaldi; Stéphane Hatem; François Lionnet; Katia Stankovic

Stojanovic; Jean-Sébastien Hulot and Richard Isnard - Cardiac dysfunction is the main mechanism

of aggravation of exercise intolerance in homozygous sickle cell disease patients.

UMRS INSERM-UPMC 1166 & ICAN

University Paris 6, Faculté de Médecine Pierre et Marie Curie, Paris, France

Department of Cardiology, Assistance Publique – Hôpitaux de Paris, Pitié-Salpêtrière Hospital, Paris, France

[37] JEZIOROWSKA Dorota1,2, Vincent Fontaine1, Charlene Jouve1, Louise Greetham1 and Jean-

Sebastien Hulot1,2 - Direct comparison of iPS monolayer vs. aggregation-based differentiation

protocols 1ICAN Institute, Paris, France 2UMRS 1166

[38] KORMANN Raphael, N. Prakoura, P. Kavvadas and C. Chatziantoniou - Inhibition of periostin

protects against the nephrotoxic serum nephritis in mice.

UMR1155

[39] LIABOTIS Athanasia1, Elisa Gomez-Perdiguero1, Ariane Galaup1, Clément Faye2, Sylvie Ricard-

Blum2, Catherine Monnot1 and Stéphane Germain1 - Molecular mechanisms of ANGPTL4-induced

regulation of vascular integrity 1Centre Interdisciplinaire de Recherche en Biologie, INSERM U1050, Collège de France 2Institut de Biologie et Chimie des Protéines, UMR 5086 CNRS - Université Lyon 1

[40] MAMELLE Elisabeth1,2,3*, Naila El Kechai4, Benjamin Granger2,5, Olivier Sterkers1,2,3, Amélie

Bochot4, Florence Agnely4, Evelyne Ferrary1,2,3 and Yann Nguyen1,2,3 - Effect of middle ear applied

dexamethasone gel on hearing after manual or motorized cochlear implantation in guinea pig 1UMR S-1159, Inserm / UPMC, “Minimally invasive robot-based hearing rehabilitation”, 75013 Paris France 2Sorbonne University, UPMC, Paris 6, Paris, France 3AP-HP, Pitie-Salpêtrière Hospital, Otolaryngology Department, Unit of Otology, Auditory implants, and Skull

base surgery, 75013 Paris, France 4Institut Galien Paris Sud, CNRS 8612, Univ. Paris-Sud, Paris-Saclay University, 92290 Chatenay-Malabry, France 5AP-HP, Pitie-Salpêtrière Hospital, Department of Public Health, 75013 Paris, France

[41] PAIVA Solenne, Pierre Joanne and Onnik Agbulut - Epigenetic factors for enhanced maturation

of cardiomyocytes derived from human pluripotent stem cells for cardiac tissue engineering

Université Pierre et Marie Curie - Paris 6

[42] PERRA Lea, Viviane Balloy, Sarah Fedele, Harriet Corvol, Michel Chignard and Loic Guillot - Role

of CHAC1 (ChaC Glutathione-Specific Gamma-Glutamylcyclotransferase 1) in the modulation of

CF (Cystic Fibrosis) bronchial epithelial cell response infected with Pseudomonas aeruginosa

INSERM, UMR_S 938, CDR Saint-Antoine, Paris, FRANCE, Sorbonne Universités, UPMC Univ Paris 06, UMR_S 938,

CDR Saint-Antoine, Paris, FRANCE, Pneumologie pédiatrique, AP-HP, Hôpital Trousseau, Paris, France.

[43] RAGOT Hélène, Sabine Guinemer, Inès Da Costa, Evelyne Polidano, Régine Merval, Christos

Chatziantoniou2 and Jane-Lise Samuel - Notch3 null mice show deficient cardiac adaptation to

moderate exercise

UMRS 942, Hôpital Lariboisière, PARIS 2UMRS 1155, Hôpital Tenon, PARIS

[44] RAHHAL Amer1, Slawomir Kusmia2, Fabrice Atassi1, Myriam Berthet1, Alban Redheuil2,Nadjia

Kachenoura2 and S. N. Hatem1 - Role of Epicardial Adipose Tissue in the Pathophysiology of Atrial

Fibrillation 1UPMC Univ Paris 06, INSERM 1166, Sorbonne Universities, Paris. 2UPMC Univ Paris 06, INSERM 1146, CNRS 7371, Laboratoire d’Imagerie Biomédicale, Sorbonne Universities,Paris.

[45] ROSENBAUM David (1,2,3), Antonio Gallo (1,2), Alessandro Mattina (1,2), Edouard Koch (4),

Florence Rossant (5) Nadjia Kachenoura (2,3), Michel Paques (4), Alban Redheuil (2,3,6) and Xavier

Girerd (1,3) - Retinal Arterioles Wall-To-Lumen-Ratio Changes in Humans as Assessed by Adaptive

Optics Camera

(1) Preventive Cardiovascular Unit, Groupe Hospitalier Universitaire Pitie-Salpêtrière, Assistance Publique-

Hôpitaux de Paris, Paris, France.

(2) Sorbonne Universités, UPMC Univ Paris 06, INSERM 1146, – CNRS 7371, Laboratoire d’imagerie Biomédicale,

F-75013, Paris, France.

(3) Institute of Cardiometabolism and Nutrition, ICAN, Paris, France

(4) Unité INSERM 968 Institut de la vision - Centre d’Investigation Clinique 503 Centre Hospitalier National des

Quinze-Vingts, Assistance Publique-Hôpitaux de Paris, Paris, France.

(5) ISEP, Paris

(6) Département d’imagerie cardiovasculaire et de radiologie interventionnelle, Pôle Imagerie - Groupe

Hospitalier Pitie-Salpêtrière, Assistance Publique-Hôpitaux de Paris, Paris, France.

[46] SALEM Joe-Elie MD ‡§, Marine Germain*‡, Beny Charbit*, MD, PHD#, Pascal Voiriot, MD II,

Bruno Lebourgeois, MD§, Eric Dasque, RN §, Jean Waldura, PHD‖II, David-Alexandre Tregouet,

PHD‡, Christian Funck-Brentano,MD-PHD‡§ and Jean-Sébastien Hulot, MD-PHD ‡§ - GENomE Wide

Analysis of Sotalol-induced IKr inhibition during ventricular REPOLarization, “GENEREPOL study”: Lack

of common variants with large effect sizes.

‡ Sorbonne-Universités, UPMC Univ Paris 06, INSERM, UMRS-1166, Institute of Cardio metabolism and Nutrition

(ICAN), Paris, France

§ AP-HP, CIC-1421-Paris-Est, Pitie-Salpêtrière Hospital, F-75013, Paris, France

II‖ Cardiabase-Banook group, Nancy, France.

# Anesthesia-Reanimation department, Hôpital Robert Debré, Reims, France.

[47] SERBIN Bettina, Mumtaz R, Trepiccione F, Hennings JC, Huebner AK, Ullah SA, Paunescu T,

Capen D, Lashhab RM, Mouro-Chanteloup I, Alper SL, Wagner CA, Cordat E, Brown D, Eladari D

and Hübner CA - Type A intercalated cell depletion and V-ATPase mistargeting in AE1 R607H

knock-in mice modeling human dominant distal renal tubular acidosis 1Institute of Human Genetics, Jena University Hospital, Friedrich Schiller Universität, Jena, Germany 2INSERM U970, Paris Cardiovascular Research Center ; Université Paris Descartes, Department of Physiology,

European Hospital Georges Pompidou, Paris, France 3Department of Physiology, University of Alberta, Edmonton, Alberta, Canada 4Center for Systems Biology, Massachusetts General Hospital, Boston and Program in Membrane Biology,

Harvard Medical School, Boston and Division of Nephrology, Harvard Medical School, Boston, USA 5Institut National de la Transfusion Sanguine, Paris, France, Inserm, UMR_S665, Paris, France, Université Paris

Diderot, Sorbonne Paris Cité, Paris, France, Laboratory of Excellence GR-Ex., Paris, France 6Renal Division and Molecular and Vascular Medicine Division, Beth Israel Deaconess Medical Center;

Department of Medicine, Harvard Medical School, Boston, USA 7Institute of Physiology, University of Zurich, Zurich, Switzerland

[48] SONNEVILLE Florence¹, M. Ruffin¹, P. Le Rouzic¹, H. Corvol¹ and O. Tabary¹ - miR-9 and ANO1:

therapeutic targets in cystic fibrosis

CDR Saint-Antoine, Paris, France

[49] TANNOUS Cynthia1, Jocelyne Blanc1, Nathalie Mougenot2-3, Arnaud Ferry2, Stéphane Hatem2-3,

Zhenlin Li1 and Mathias Mericskay1 - Role of nicotinamide riboside kinase 2 in dilated

cardiomyopathy 1Institute of Biology Paris-Seine, Université Pierre et Marie Curie Paris 6, Dept of Adaptation and Ageing Biology

(CNRS UMR 8256 / Inserm ERL U1164) (Paris, France) 2ICAN, Plateau d'Expérimentation Coeur, Muscle, Vaisseaux, GH Pitié Salpétrière, Université Pierre et Marie

Curie Paris 6 (Paris, France) 3ICAN, Génétique, Physiopathologie & Pharmacologie Cardiovasculaire INSERM U956, Université Pierre et

Marie Curie Paris 6 (Paris, France)

[50] TIAN Lei - Role of integrin αv and transcription factor SRF in the vascular stiffness

UPMC Univ Paris 06, CNRS UMR8256/INSERM ERL U1164

[51] TORRES LAZO Victor Renato MD1,2,3, Guillaume Kazmitcheff PhD1,3,4, Daniele De Seta MD1,2,3,

Evelyne Ferrary MD, PhD1,2,3, Olivier Sterkers MD, PhD1,2,3, Yann Nguyen MD, PhD1,2,3 - Improvement of

the variability of the insertion axis to the scala tympani by a robotic semi-automatic system in

cochlear implantation 1UMR-S 1159 “Minimally Invasive Robot-based Hearing Rehabilitation”, Inserm, Paris 6 UPMC, Paris France 2Sorbonne Universities, UPMC Univ. Paris 6, Paris, France 3Otolaryngology Department, Unit of Otology, Auditory Implants and Skull Base Surgery, AP-HP, Pitié-Salpêtrière

Hospital, Paris, France 4Shacra Inria, Lille Nord-Europe, Université Lille-1, Lille, France

[52] VOISIN Sarah, Wu Q, Jouin M, Pattou F, Six MF, Patrice A, Junien C, Gabory A - Methylome and

transcriptome analysis of abdominal muscle in type 2 diabetic women

UMR BDR, INRA, Domaine de Vilvert, 78350 Jouy en Josas, France. Ecole Doctorale 394 “Physiologie,

physiopathologie et thérapeutique”,Université Pierre et Marie Curie, 75252 Paris, France

POSTERS

Thursday, 26th May 2016 – 10:15 to 11:30

[1] BALBINO Bianca, Pierre Bruhns and Laurent Reber - Pathways of peanut anaphylaxis in a

'humanized' mouse model

Institut Pasteur

[2] BONNET Benjamin1,2,3,4, James Vigneron1,2,3, Béatrice Levacher1,2,3, Thomas Vazquez1,2,3, Fabien

Pitoiset1,2,3, Faustine Brimaud1,2,3, Guillaume Churlaud1,2,3,4, David Klatzmann1,2,3,4, Bertrand

Bellier1,2,3,4 - Low-dose interleukin-2 induces regulatory T-cell mediated control of experimental

food allergy 1Sorbonne Universités, UPMC Univ Paris 06, UMRS_959, I3, F-75013, Paris, France 2INSERM, UMRS_959, I3, F-75013, Paris, France 3CNRS, FRE3632, I3, F-75013, Paris, France 4AP-HP, Groupe Hospitalier Pitie-Salpêtrière, Department of Biotherapies and Clinical Investigation Center in

Biotherapy, F-75013, Paris, France.

[3] CANESI Fanny, Vimala Diderot, Dominique Couchie, Mustapha Rouis & Khadija El Hadri -

Thioredoxin-Mimetic Peptides: New Promising Therapeutic Strategyfor the Treatment of

Cardiovascular Diseases

UMR 8256 - B2A - Biological Adaptation and Ageing ; UPMC ; INSERM ; CNRS

[4] CONART Jean-Baptiste, Xavier Guilloneau, Pascale Massin and Florian Sennlaub - Cone

segment loss in retinal detachment

Sorbonne Université, UPMC Univ Paris 06, INSERM, CNRS, Institut de la Vision, Unité 968, 17 rue Moreau, 75012

Paris, France.

[5] DAS Mrinmoy, Maxime Lecerf, Srini V Kaveri and Jagadeesh Bayry - Induction of autophagy in

immune cells by Intravenous Immunoglobulin.

Centre de Recherche des Cordeliers, Equipe 16 - Immunopathology and therapeutic immunointervention,

Paris, F-75006, France

[6] DIALLO Mariama1, Samri, A.1, Even, S.1, Charpentier, C.2, Matheron, S.3, Brinvezinet, F.2, Autran,

B.1 - Distribution of HIV-2 Reservoir in Cd4 + Cells Patient Infected with HIV-2 1Sorbonne Universités, UPMC Univ Paris 06, CIMI - Paris, F-75013, France; Inserm, U1135, CIMI- Paris, Paris, F-

75013, France; AP-HP, Hôpital Pitié-Salpêtrière, Département d’Immunologie, Paris, F-75013, France 2AP-HP, Hôpital Bichat-Claude Bernard, Laboratoire de Virologie EA 4409, Paris, F- 75018, France ; Université

Paris-Diderot, Sorbonne Paris-Cité, Faculté de Médecine. 3AP-HP, Hôpital Bichat-Claude Bernard, Service de Maladies infectieuses et tropicales, Paris, F- 75018,

France ; Université Paris-Diderot, Sorbonne Paris-Cité, Faculté de Médecine.

[7] DIVOUX Jordane, Vallion, R., Ronin, E., Lubrano di Rocco, M., Preato, C., Gregoire, S., Marodon,

G., Banderas, A. and Salomon, B. - Obesity induced inflammation: impacts on immune cells in

visceral adipose tissue

CIMI U1135

[8] DONG Yuan*†, J. Lagarde‡, H. Corne‡, Y. Chantran*†, P. Aucouturier*†, G. Dorothée†, M.

Sarazin‡ and C. Elbim*† - Phenotypic and functional characterization of neutrophils in Alzheimer

disease: association with disease severity

*Sorbonne Universités, UPMC Univ Paris 06, Paris, France ;

†INSERM, Centre de Recherche Saint-Antoine, UMR-S 938, Paris, France ;

‡AP-HP, Hôpital Saint-Anne, Unité de neurologie de la mémoire et du langage, Paris, France. [9] DRARENI Karima, Amine Toubal, Rapahelle Ballaire, Eckardt Treuter and Nicolas Venteclef -

Epigenomic control of adipose tissue function and energy metabolism in obesity and type 2

diabetes

Equipe 8 - pathogenèse cellulaire et clinique du diabète

[10] EYMARD Florent1,2, Audrey Pigenet1, Danièle Citadelle1, Joan Tordjmann3, Charles-Henri

Flouzat Lachaniette4, Karine Clément3, Francis Berenbaum1,5, Xavier Chevalier2 and Xavier

Houard1 - Knee and hip intra-articular adipose tissues share a common phenotype in osteoarthritis 1INSERM UMR-S 938, UPMC, Saint Antoine research center, F-75571 Cedex 12, Paris, France. 2Department of Rheumatology, AP-HP Henri Mondor Hospital, F-94010, Créteil Cedex, France. 3INSERM U1166, UPMC, Cordeliers research center, 75006, Paris, France 4Department of Orthopedic Surgery, AP-HP Henri Mondor Hospital, F-94010, Créteil Cedex, France. 5Department of Rheumatology and “Inflammation-Immunopathology-Biotherapy” (DHU i2B), AP-HP Saint-

Antoine Hospital, F-75012 Paris, France.

[11] GALEOTTI Caroline (1, 2, 3, 4), Hedge P (1,3), Das M (1,2,3), Stephen-Victor E (1,2,3), Canale F

(1,3), Munoz M (1,3), Sharma VK (1,3), Dimitrov JD (1,2,3,5), Kaveri SV (1,2,3,5,6) and Bayry J

(1,2,3,5,6) - Heme oxygenase-1 is dispensable for the anti-inflammatory activity of intravenous

immunoglobulin

(1) Institut National de la Santé et de la Recherche Médicale Unité 1138, Paris, F-75006, France

(2) Sorbonne Universités, UPMC Univ Paris 06, UMRS 1138, Paris, F-75006, France

(3) Centre de Recherche des Cordeliers, Equipe-Immunopathology and theraeutic immunointervention,

Paris, F-75006, France

(4) department of Pediatric Rheumatology, National Referral Centre of Auto-inflammatory Diseases, CHU de

Bicêtre, Le Kremlin Bicêtre, F-94270, France

(5) Université Paris Descartes, Sorbonne Paris Cité, UMRS 1138, Paris, F-75006, France

(6) International Associated Laboratory IMPACT , National Institute of Immunohaematology, Mumbai, 400012,

India

[12] GEA-MALLORQUI Ester, Mabel Jouve, Nicolas Ruffin, Laurent Zabloki, Mathieu Maurin and

Philippe Benaroch - HIV-2 infection in Human Macrophages.

U932 Institut Curie.

[13] GONNET Jessica1, Weiss L.1,2, Boccara D.1,3, Cardinaud S.1, Yahia N.1, Dufossée M.1, Wagner

R.4, Verrier B.5, Moris A.1, Vogt A.1,2,Mimoun M.3, Combadière B.1 and Perrin H.1 - IL-32 role in

antigen-specific T cell responses after MVA administration in human skin 1Centre d’Immunologie et des Maladies Infectieuses-Paris (Cimi-Paris), Inserm U1135, Sorbonne Universités

UPMC université Paris 06 UMRS CR7 2Clinical Research Center for Hair and Skin Science, Department of Dermatology and Allergy, Charité-

Universitätsmedizin Berlin, Berlin, Germany 3Service de chirurgie plastique reconstructrice, esthétique, centre des brûlés, hopital Saint-Louis, Assistance

Publique Hôpitaux de Paris 4Fachgruppe Physik, Bergische Universit¨at Wuppertal, 42097 Wuppertal, Germany 5Institut de Biologie et Chimie des proteins UMR 5305, CNRS/Université de Lyon.

[14] Bagirath Gangadharan1,2,3, ING Mathieu1,2,3, Sandrine Delignat1,2,3, Ivan Peyron1,2,3, Maud

Teyssandier1,2,3, Srinivas V Kaveri1,2,3 and Sébastien Lacroix-Desmazes1,2,3 - Role of the C domains in

the immunogenicity of therapeutic factor VIII in hemophilia A 1Sorbonne Universités, UPMC Univ Paris 06, UMR S 1138, Centre de Recherche des Cordeliers, F-75006, Paris,

France; 2INSERM, UMR S 1138, Centre de Recherche des Cordeliers, F-75006, Paris, France; 3Université Paris Descartes, Sorbonne Paris Cité, UMR S 1138, Centre de Recherche des Cordeliers, F-75006,

Paris, France.

[15] JAILLET Cyprien*, Willy Morelle°, Pierre Martinez°, Marie-Christine Slomianny°, Valérie Buard*,

Fanny Caffin*, Marc Benderitter*, Christian Slomianny°°, Anne-Sophie Lacoste°°, François

Foulquier°, Agnès François*, Fabien Milliat*, Fabrice Allain° and Olivier Guipaud* - Role of

endothelial cell glycosylation in the initiation and development of radiation tissue injury

*IRSN, PRP-HOM/SRBE/L3R, 92260 Fontenay-aux-Roses;

°UGSF, UMR8576

°°Bio Imaging Center, Inserm U1003, Université Lille 1, 59655 Villeneuve D’Ascq, France

[16] Le MOIGNIC Aline, Maude Guillot-Delost, Claude Baillou, Patrick Midoux, François Lemoine

and Véronique Mateo - Preclinical validation of new therapeutic anti-cancer vaccine targeting

dendritic cells by using RNA modified lipopolyplexes

CIMI - Centre de recherche d'Immunologie et Maladies infectieuses ; UMRS CR7, INSERM U1135, CNRS ERL

[17] Scott D. Speer, LI Wu Zhi, Béatrice Payelle-Brogard, Sofija Buta, Erminia Rubino, Sara Löchte,

Stephan Wilmes, Jacob Piehler, Dusan Bogunovic and Sandra Pellegrini - Fine Tuning of Type I

Interferon Response in Humans and Mice

Institut Pasteur, Paris, France ; Icahn School of Medicine at Mount Sinai, NY, NY, USA ; University of Osnabrück,

Osnabrück, Germany

[18] LUBRANO DI RICO Martina, Sylvie Gregoire, Benoit Salomon - Role of TNFR family on regulatory

T cells.

INSERM-CNRS-UPMC

[19] LUQUE Yosu1,2,3, Dominique Cathelin1,2, Sophie Vandermeersch1,2, Xiaoli Xu1,2, Julie Sohier1,2,

Sandrine Placier1,2, Alexandre Hertig1,2,3, Jean-Christophe Bories4, Florence Vasseur5, Fabien

Campagne6, James P. Di Santo7, Christian Vosshenrich7, Eric Rondeau1,2,3 and Laurent

Mesnard1,2,3,6 - Glomerular common gamma chain confers B and T cell-independent resistance to

glomerulonephritis 1Sorbonne Universités, UPMC Univ Paris 06, UMR_S 1155, “Rare and Common Kidney Diseases, Matrix

Remodeling and Tissue Repair”, F-75005, Paris, France 2Inserm UMR 1155, “Rare and Common Kidney Diseases, Matrix Remodeling and Tissue Repair”, Hôpital

Tenon, F-75020, Paris, France 3APHP, Urgences Néphrologiques et Transplantation Rénale, Hôpital Tenon, F-75020, Paris, France 4Inserm UMR 1126, Institut Universitaire d'Hématologie, Hôpital St. Louis, Paris, France 5Inserm U1020, Université Paris Descartes, 75014 Paris, France 6Weill Medical College of Cornell University, Institute of Computational Biomedicine, New York, NY 10065, USA 7Institut Pasteur, Unité Immunité innée and Inserm U668, 75724 Paris, France

[20] MONSEL Antoine, Lucrèce Aimade, Olivier Langeron, David Klatzmann, Michelle Rosenzwajg -

Temporal and compartment dynamics of immune phenotypes in acute respiratory distress

syndrome Multidisciplinary Intensive Care Unit, Department of Anesthesiology and Critical Care, La Pitie-Salpêtrière

Hospital, Assistance Publique-Hôpitaux de Paris

Laboratoire Immunologie-Immunopathologie-Immunothérapie Equipe ImmunoPhysiopathologie (iP) UPMC

UMR 7211 - CNRS FRE3632 - INSERM U959

[21] OUHACHI Melissa, Martine Moreau, Philippe Lesnik, Thierry Huby, Emmanuel Gautier - IRF4-

dependent CD11b+ dendritic cells controls the polarization of Th cells in atherosclerosis.

INSERM U1166.

[22] RONIN Emilie, Rouers A, Pouchy C, Grégoire S, Zaragoza B, Burlion A, Weih F, Baeyens A,

Salomon B - Role of NF-kB in the biology of FoxP3+ regulatory T cells at steady state and during

inflammation

UPMC/Inserm/CNRS

[23] TCHOUKAEV Anastasia1,4, J. Taytard1,3,4, C. Rebeyrol1,4, F. Sonneville1,4, P. Bardin1,4, D. Debray1,

N. Rousselet1,4, S. Blouquit-Laye2, L. Guillot1,4, H. Corvol1,3,4, N. Chignard1,4, O. Tabary1,4 and P. Le

Rouzic1,4 - Regulation of corticosteroid-binding globulin (CBG) in the inflammatory context of

cystic fibrosis. 1UMR_S938 Inserm, 2Université Versailles, Saint-Quentin en Yvelines, 3Hôpital Armand Trousseau, Paris, 4Université Paris 06, Paris.

[24] TOUHAMI Sara, Sébastien Augustin, Xavier Guillonneau and Florian Sennlaub - Age-related

Macular Degeneration and Sleep Apnea Institut de la Vision, UMRS 968

[25] TRAN Sophie, Lucie Poupel, Melissa Ouhachi, Thierry Huby, Wilfried Le Goff, Emmanuel Gautier

- Deciphering the role of liver macrophage subsets in cardiometabolic diseases.

INSERM UMRS_1166

[26] URRUTIA Alexandra1,2,*, Darragh Duffy1,2,3,*, Vincent Rouilly3, Céline Posseme3, Raouf Djebali3,

Gabriel Illanes3,4,5, Valentina Libri3, Benoit Albaud6, David Gentien6, Barbara Piasecka3, Milena

Hasan3, Magnus Fontes4,7*, Lluis Quintana-Murci8,9,*, Matthew L. Albert1,2,3,10,* for The Milieu Intérieur

Consortium† - Standardized whole-blood transcriptional profiling enables the deconvolution of

complex induced immune responses 1Laboratory of Dendritic Cell Immunobiology, Department of Immunology, Institut Pasteur, Paris France 2INSERM U818, Paris France 3Center for Human Immunology, Institut Pasteur, Paris France 4IGDA, Institut Pasteur, Paris France 5Centro de Matemática, Facultad de Ciencias, Universidad de la República, Uruguay. 6Institut Curie, Centre de Recherche, Département de recherche translationnelle, Plateforme de

Génomique, Paris, France 7Centre for Mathematical Sciences, Lund University, Lund, Sweden 8Laboratory of Human Evolutionary Genetics, Department of Genomes & Genetics, Institut Pasteur, Paris

France 9CNRS URA3012, Paris France 10Department of Cancer Immunology, Genentech Inc, San Francisco CA

[27] VILLEGAS VAZQUEZ Jose, Le Panse R, Berrih-aknin S and Dragin N - Expression of Interleukin-23

in Thymuses of Myasthenia Gravis Patients

Center of Research in Myology, Sorbonne Universités, UPMC - Inserm UMRS 974, CNRS FRE3617, Institute of

Myology, G.H. Pitie-Salpêtrière, Paris, France.

[28] ZABLOCKI Laurent1, Aditi Varthaman1, Francois-Xavier Gobert1, Samuel Menzies2, Paul Lehner2,

Nicolas Manel1 and Philippe Benaroch1 - Analysis of the molecular mechanisms of innate immune

response using a genome wide genetic screen.

1Institut Curie-INSERM U9321, 12 rue Lhomond, 75005 Paris, France ; 2Cambridge Institute for Medical Research2, Addenbrooke’s Hospital, Cambridge, United Kingdom

POSTERS

Thursday, 26th May 2016 – 16:15 to 17:30

[29] BERTAUX Audrey, Cabon L., Brunelle M. N. and Susin S. A. - Control of mitochondrial OXPHOS

and metabolism by AIF is essential for hematopoiesis

Centre de Recherche des Cordeliers UMRS 1138

[30] BOUFTAS Nora, Nikalayevich Elvira, Wassmann Katja - Regulation of chromosome

segregation in mammalian oocytes.

Mammalian Oocyte Meiosis -MOM (Wassmann lab)- UMR7622

[31] BRUNEAU Alix1*, Jean-Louis Delaunay1*, Brice Hoffmann2, Anne-Marie Durand-Schneider1,

Véronique Barbu1, Chantal Housset1, Michèle Maurice1, Isabelle Callebaut2, Tounsia Aït Slimane1

- Phenotypic analysis of function-defective ABCB4 mutants: Effect of correcting molecules 1Centre de Recherche saint-Antoine , INSERM/UPMC, 27 rue Chaligny, Paris 75012, France 2IMPMC, UMR7590, CNRS-UPMC, MNHN, IRD, Paris, 75005, France

* Equal contribution

[32] CANLORBE Geoffroy1,2,3, Zhe Wang1, Enora Laas2, Sofiane Bendifallah2,4, Mathieu Castela1,

Marine Lefevre5, Nathalie Chabbert-Buffet1,2, Emile Daraï1,2,3, Selim Aractingi1, Céline Méhats6,7

and Marcos Ballester1,2,3,7 - Identification of microRNA expression profile related to lymph node

status in women with early-stage grade 1–2 endometrial cancer 1INSERM, UMR S 938, University Pierre et Marie Curie, Paris, France; 2Department of Obstetrics and Gynaecology, Tenon University Hospital, Assistance Publique des Hôpitaux

de Paris (AP-HP), University Pierre and Marie Curie, et Paris, Paris, France; 3Institut Universitaire de Cancérologie (IUC), Paris, France; 4INSERM UMR S 707, Epidemiology, Information Systems, Modeling, University Pierre and Marie Curie, Paris,

France; 5Department of Pathology, Tenon University Hospital, University Pierre and Marie Curie, Paris, France

6Cochin Institute, Inserm U1016, CNRS 8104, Université Paris Descartes, Paris, France

[33] COURTIES Alice1, Alain Sautet2, Francis berenbaum1 and Jérémie Sellam1 - The non-neuronal

cholinergic system: a new actor involved in osteoarthritis pathophysiology. 1Rheumatology Department, Saint-Antoine Hospital, Inserm UMR S_938, UPMC Univ Paris 06, Assistance

Publique–Hôpitaux de Paris (AP-HP), Paris, France 2Department of surgical orthopaedic, Saint-Antoine Hospital, Assistance Publique–Hôpitaux de Paris (AP-

HP), Paris, France

[34] DACLAT Rita and Jean-Marc Lacorte - Postprandial modulation of circulating microRNA in

hypertriglyceridemic patients

UMRS Inserm/UPMC 1166-Equipe 4

[35] DALLE Héloïse, Marie Garcia, Tatiana Ledent, Marthe Moldes and Bruno Feve - The role of

adipose glucocorticoid receptor in corticosterone-induced lipodytrophy.

Lipodystrophies génétiques et acquises INSERM-UMR_S 938

[36] GENSER Laurent1,2,6, Sabrina Benaïssa1,3, Adriana Torcivia6, Monique Rousset1,3, Karine

Clément1,2,4, Edith Brot-Laroche1,3 , Armelle Leturque1,3, Sophie Thenet1,3,5* , Christine Poitou1,2,4* -

Impairment of Intestinal Barrier Integrity in Human Obesity: Involvement of Dietary Lipids 1Institute of Cardiometabolism and Nutrition, ICAN, Pitie-Salpêtrière Hospital, Paris, F-7513, France; 2UMR 1166 team 6 INSERM UPMC UPD, Pitie-Salpêtrière Hospital, Paris, F-75013 France 3UMR 1138 INSERM UPMC UPD, Cordeliers Research Center, F-75006 Paris; 4Assistance Publique-Hôpitaux de Paris, Pitie-Salpêtrière Hospital, Heart and metabolism department Paris,

F-75013 France; CRNH-Ile de France, Paris, F-75013 France; 5EPHE, PSL Research University, F-75006 Paris; 6Department of digestive surgery, liver transplantation, Pitie-Salpêtrière Hospital.

[37] GIABICANI Eloïse - Physiopathology of Insulin like growth factor 1 receptor

UMR_S938 Hôpital Armand Trousseau, 26 rue du Dr A. Netter, 75012 Paris

[38] GRANJON David1,2, Olivier Bonny2 and Aurélie Edwards1 - A model of Ca/Pi homeostasis. 1Equipe 3 Métabolisme et Physiologie Rénale, Centre de Recherche des Cordeliers, Paris 2Département de Pharmacologie et Toxicologie, Université de Lausanne, Lausanne, Suisse

[39] HANOUNA Guillaume, Laurent Mesnard, Sophie Vandermeersch, Joëlle Perez, Sandrine

Placier, Jean-Philippe Haymann, Aurélien Bataille, Laurent Baud, Emmanuel Letavernier -

Specific calpain inhibition protects against inflamm-aging.

Sorbonne universites-UPMC Univ Paris 06, UMR S 1155, F-75020, Paris, France ; INSERM, UMR S 1155, F-75020,

Paris, France ; AP-HP, Hôpital Tenon, Explorations fonctionnelles multidisciplinaires 75020, Paris, France

[40] KEMGANG Astrid - Contribution of gut microbiota in Primary Sclerosing Cholangitis (PSC)

Metabolic and biliary fibro-inflammatory diseases of liver (Pr Housset)

[41] LE GUILCHER Camille1,2, Garcin Isabelle1, Tebbi Ali3, Besnard Aurore1, Doignon Isabelle1,

Julien Boris1 and Tordjmann Thierry1 - The purinergic receptor P2X4 regulates liver fibrogenesis

through the modulation of myofibroblast activation and inflammatory response 1INSERM U1174, Université Paris Sud 91400 Orsay ; 2UPMC Université Paris 6 75005; 3 Affymetrix eBioscience 140 B Rue de Rennes,75006 Paris.

[42] LOEUILLARD Emilien, Haquima El Mourabit, Chantal Housset and Axelle Cadoret - Inhibitory

effect of endoplasmic reticulum stress in portal myofibroblasts on liver fibrogenesis

UMRS 938 CDR Saint Antoine Maladies fibro-inflammatoires d’origine métabolique et biliaire

[43] MA Feng - HDL function as an acceptor of surface fragment of TGRL: Mechanisms and

pathophysiological relevance

Biologie intégrative de l'athérosclérose

[44] MESDOM Pierre1, Andrei Baiceanu1,2, Isabelle Hainault1, Marie Lagouge1 and Fabienne

Foufelle1 - The Role of PRDM16 in Liver Fibrosis 1UMRS 1138 Centre de Recherche des Cordeliers, département pathogénèse cellulaire et clinique du

diabète, Paris, France. 2University of Medicine and Pharmacy "Iuliu Hațieganu", Faculty of Pharmacy, Cluj-Napoca, Romania.

[45] MOURI Sarah1,2, H El-Mourabit1,2, C Rey1,2, R Morichon3, D Wendum1,2,4, E Lasnier5, C

Housset1,2,6 , N Weiss1,2,7 and D Thabut1,2,8 - Blood brain barrier permeability is increased in

hepatic encephalopathy related to cirrhosis, through a hyperammonemia-dependent

mechanism 1Sorbonne Universités, UPMC Univ Paris 06, CDR Saint-Antoine & Institute of Cardiometabolism and Nutrition

(ICAN), Paris, France;

2INSERM, UMR_S 938, Paris, France; 3Institut Fédératif de Recherche en Santé, Saint-Antoine IFR-65, Paris, France; 4Assistance Publique-Hôpitaux de Paris, Hôpital Saint-Antoine, Service d’Anatomo-Pathologie, Paris, France; 5Assistance Publique-Hôpitaux de Paris, Hôpital Saint-Antoine, Service de Biochimie; 6Assistance Publique-Hôpitaux de Paris, Hôpital Saint-Antoine, Centre de Référence des Maladies

Inflammatoires des Voies Biliaires (CMR MIVB) & Service d’Hépatologie, Paris, France; 7Assistance Publique- Hôpitaux de Paris, Hôpital Pitié Salpétrière, Unité de Soins Intensifs de Neurologie; 8Assistance Publique-Hôpitaux de Paris, Hôpital Pitié Salpétrière, Service d’Hepato-Gastroentérologie, Paris,

France [46] NICOLAS Anthony1,2, Kamel Mohammedi1,3, Naima Bellili-Muñoz1, Ronan Roussel1,3,4, Samy

Hadjadj5, Michel Marre1,3,4, Gilberto Velho1, Frédéric Fumeron1,4 - T-cadherin gene (cdh13)

polymorphisms and nephropathy in subjects with type 1 diabetes 1INSERM UMRS1138, Paris, France 2Université Pierre et Marie Curie, Sorbonne Universités, Paris, France 3Dept. Of Diabetology, Endocrinology and Nutrition, Bichat Hospital, APHP, Paris, France 4Université Paris Diderot, Sorbonne Paris Cité, Paris, France 5Dept. Of Diabetology and Endocrinology, University Hospital of Poitiers, Poitiers, France

[47] RIBAULT Alexandre, Stephane Flamant, Marc Benderitter and Radia Tamarat - Exosomes

therapeutic efficiency in the treatment of musculo-cutaneous radiation-induced damages

IRSN - Laboratoire de Rehcerhche en Régénération des Tissus Sains Irradiés

[48] ROUILLE THOMAS1,2, Natacha Kadlub3,4, Alexandre How-Kit5, Sylvie Fraitag6, Romain H.

Fontaine1,2, Selim Aractingi1,3,7 and Sarah Guégan1,2,8 - NRAS mutation and downstream signaling

pathways in congenital melanocytic pathways 1INSERM U938, Saint Antoine Research Center, Paris; 2Université Pierre et Marie Curie-Paris VI, Paris; 3Université René Descartes-Paris V, Paris, France; 4Hôpital Necker, Department of Maxillofacial and Plastic Surgery, Paris, France; 5Laboratory for Functional Genomics, Fondation Jean Dausset – CEPH, Paris, France; 6Hôpital Necker-Enfants-Malades, Department of Pathology, Paris; 7Hôpital Cochin, Department of Dermatology, Paris; 8Hôpital Tenon, Department of Dermatology, Paris.

[49] SAGET Sarah1, Lyvianne Decourtye1, Rong Cong1, Marie-Laure Endale2, Marthe Moldes1,

Laetitia Dinard1, David Tregouet2, Bruno Fève1,3, Yves Le Bouc1,4 and Laurent Kappeler1 -

Epigenetic modifications in liver are associated with metabolic alterations in mice born with

IUGR 1Sorbonne Universités, Univ Paris 06 UMR S938 and INSERM, Unité 938 and Institute of Cardiometabolism and

Nutrition (ICAN) and CDR Saint-Antoine, F-75012, Paris, France; 2Sorbonne Universités, Univ Paris 06 UMR S1166, INSERM, Unité 1166 and Institute of Cardiometabolism and

Nutrition (ICAN), F-75013, Paris, France; 3AP-HP, Hôpital Saint Antoine, F-75012, Paris, France; 4AP-HP, Hôpital Armand Trousseau, F-75012, Paris, France;

[50] SANCHEZ Manuel1, K. Mohammedi1,6, N. Bellili-Muñoz1, S. Hadjadj2,3,4, M. Marre1,5,6, R.

Roussel1,5,6 and G. Velho1 - DNA Oxidation and Diabetic Nephropathy in People with Type 1

Diabetes 1INSERM, Research Unit 1138, Centre de Recherche des Cordeliers, Paris, France; 2Université de Poitiers, CIC1402, Poitiers, France; 3CHU Poitiers, pole DUNE, Poitiers, France; 4INSERM, Research Unit 1082, Poitiers, France; 5Diabetology Endocrinology Nutrition, DHU FIRE, Bichat Hospital, Paris, France; 6University Paris Diderot, Department of Medicine, Paris, France

[51] SCHMITT Charlotte1, Thomas Aranias1, Véronique Carrière1, Kévin Garbin1, Maude Le Gall2,

Edith Brot-Laroche1, Armelle Leturque1, Alexandra Grosfeld1 and Patricia Serradas1 - Intestinal

GLUT2 invalidation leads to glucose malabsorption and decreased GLP-1 cell density 1Inserm UMR_S 1138, Centre de Recherche des Cordeliers; Sorbonne universités, UPMC Univ Paris 06;

Sorbonne Cités, UPD Univ Paris 05; F-75006, Paris, France 2Inserm UMR_S 1149, DHU Unity; Sorbonne Cités, UPD Univ Paris 05, F-75890, Paris, France

[52] TOUCH Sothea1,2,3, Christine Poitou1,2,3,4, Magali Fradet3, Laurent Genser1,2,3,4, Aurélie

Gestin1,2,3, Héléna Mosbah1,2,3,4, Judith Aron-Wisnewsky1,2,3,4, Edith Brot-Laroche1,2,5, Michèle

Guerre-Millo1,2,3, Karine Clément1,2,3,4, Sébastien André1,2,3 - Functional interactions between

systemic and intestinal immunity in human obesity 1Sorbonne Universités, UPMC Univ Paris 6, UMRS 1166 and UMRS 1138, Paris, France 2INSERM, U1166 Team 6 Nutriomics, Paris, France, 3Institute of Cardiometabolism And Nutrition, ICAN, Paris, France, 4Assistance Publique Hôpitaux de Paris, AP-HP, Pitié Salpêtrière Hospital, Nutrition department, Paris, France, 5INSERM, U1138 Cordeliers Research Center, Paris, France.

[53] VALLOT Antoine, Ioanna Leontiou, Warif El Yakoubi, Damien Cladière, Eulalie Buffin and

Katja Wassmann - Quality of chromosome attachments is controlled by the spindle assembly

checkpoint in oocytes

Sorbonne Universités, Intitut de Biologie Paris Seine, CNRS UMR7622 Developmental Biology Lab, Paris 75005

France

[54] ZHANG Xufei, Devime F, Maximin E, Blottière H, Heberden C and Douard V. - Role of

intestinal homeostasis in mediating the effect of chronic intake of sugars

NIM--MICALIS--INRA Jouy-en-Josas

CONTACT LIST

1st YEAR PhD student

ATLAS Yoann yoann.atlas@free.fr

BALBINO Bianca biancabalbino@gmail.com

BANDET Cécile cecile.bandet@gmail.com

BOTTE Alexandra alexandra.botte@gmail.com

BOUFTAS Nora nbouftas@gmail.com

BOUGACHA Nadia nadia.bougacha@gmail.com

BOUVET Delphine delphine.bouvet@inserm.fr

BRUNEAU Alix alix.bruneau@hotmail.fr

CAMPION Sébastien sebastien.campion@me.com

CANESI Fanny fcanesi@free.fr

COHEN Romain romcohen@gmail.com

CONART Jean-Baptiste jbconart@gmail.com

COURTIES Alice acourties@yahoo.fr

COUTURIER Aude audecout@aol.com

DACLAT Rita rdaclat@gmail.com

DAHER Marie-Thérèse daher.marietherese@gmail.com

DALLE Héloïse heloise.dalle@orange.fr

DELOUX Robin robin.deloux@gmail.com

DIALLO Mariama nenettediallo@yahoo.fr

DIVOUX Jordane jordane-divoux@hotmail.fr

DONG Yuan jasonkiddy@163.com

DRARENI Karima karimadrareni@gmail.com

ESCRIBANO VAZQUEZ Unai unai.evo@gmail.com

GHEZZAL Sara sara.ghezzam@gmail.com

GOFAS SALAS Elena gofas.eleni@gmail.com

KORMANN Raphael raphaelkormann@gmail.com

LATTUCA Benoît benoit.lattuca@gmail.com

LE GUILCHER Camille camille-leguilcher@hotmail.fr

LOBE Cindy lobecindy@hotmail.com

LUBRANO DI RICO Martina m.lubranodiricco@gmail.com

MA Feng marc56718799@gmail.com

MAMELLE Elisabeth elisabeth.mamelle@gmail.com

MAREK Veronika CIFRE veronica.marek@polytechnique.edu

nika.marek@gmail.com

MASMOUDI Hicham hic.masmoudi@gmail.com

hicham.masmoudi@aphp.fr

MEJECASE Cécile cecile.mejecase@hotmail.fr

MOURI Sarah sarahm7513@hotmail.com

PAIN - GIABICANI Eloïse eloise.giabicani@aphp.fr

PAIVA Solenne solenne@live.com.pt

PERRA Lea lea.perra@gmail.com

PHAM Thi Minh Tam minhtamminh@gmail.com

POSTAL Barbara barbarapostal5@gmail.com

PRAMIL Elodie elodie.pramil@hotmail.fr

RAHHAL Amer dr_rahh@hotmail.com

RIBAULT Alexandre alex.ribault@gmail.com

RUSSICK Jules jules.russick@gmail.com

SALAMEH Sacha sachasalameh@hotmail.com

SANCHEZ Manuel manuel.j.sanchez@wanadoo.fr

SOYSOUVANH Fréderic soysouvanh.frederic@hotmail.fr

TABIBZADEH Nathalie tabnahid]@gmail.com

TCHOUKAEV Anastasia anastasia.tchoukaev@hotmail.fr

TIAN Lei tianlei2012@sjtu.edu.cn

TOUHAMI Sara saratouhami@gmail.com

TRAN Sophie transophie@outlook.com

URRUTIA Alexandra alejandra.urrutia@pasteur.fr

VILLEGAS VAZQUEZ Jose avillegas8427@gmail.com

2nd YEAR PhD student

ANDROUIN Alexandre alexandre.androuin@gmail.com

AYARI Sami sam-ayari@hotmail.fr

sami.ayari@crc.jussieu.fr

BAUM David Marcel david.marcel.baum@gmail.com

BEGUIER Fanny fanny.beguier@gmail.com

BENABOU Eva eva.benabou@gmail.com

BERTAUX Audrey audrey.bertaux@crc.jussieu.fr

BEURIOT Adeline beuriotadeline@gmail.com

BIGNON Yohan yohan.bignon@gmail.com

BOCCARA David davboc9@hotmail.com

BOKHARI Adem adem.bokhari@gmail.com

BONNET Benjamin benjaminbonnet@free.fr

BOUAZIZ Mehdi mehdi.bouaziz@ymail.com

BRUNEL Simon simonbrunel@live.fr

BUONAFINE Mathieu mathieu.buonafine@gmail.com

CANLORBE Geoffroy geoffroy.canlorbe@tnn.aphp.fr

CHARLES-MESSANCE Hugo hugo.charles.messance@gmail.com

CLASSE Marion marion.classe@lrb.aphp.fr

CLAUDE Olivier olivier.claude@upmc.fr

CRON Mélanie melanie.cron@etu.upmc.fr

melanie.cron@yahoo.fr

DAHLQVIST Géraldine geraldine.dahlqvist@uclouvain.be

DAJON Marion marion.d_1152@hotmail.fr

DEL RIO Iratxe iratxeRio@gmail.com

iratxe.del-rio-iniguez@pasteur.fr

DESBOIS Anne-Claire anneclairedesbois@yahoo.fr

DEZAIRE Ambre ambre.dezaire@hotmail.fr

DRES Martin martin.dres@psl.aphp.fr

EL BOUSTANY Ray ray_boustany@hotmail.com

ESTEVE Emmanuel esteve.emmanuel@gmail.com

GALEOTTI Caroline caroline.galeotti@gmail.com

GONNET Jessica jess-g@orange.fr

GREENE Malorie malorie.greene@inserm.fr

mg.12@hotmail.com

HOLLANDE Clémence clemenceho@hotmail.com

HU Mengyue mengyuehu@126.com

HUR Justine justinehur@gmail.com

JAROSSAY Annaelle jarossay.annaelle@gmail.com

KAPLON Hélène helene.kaplon@gmail.com

KEMGANG FANKEM Astrid Donal kastriddonald@yahoo.fr

LAUNOIS Claire launois.claire@gmail.com

LAVIGNE Jeremy jeremy.lavigne@orange.fr

LEBRETON Guillaume guillaume.lebreton@psl.aphp.fr

LEMALE Julie julie.lemale@trs.aphp.fr

LIABOTIS-FONTUGNE Ahanasia a.liabotisf@gmail.com

LIVROZET Marine marinelivrozet@gmail.com

LOPEZ CAYUQUEO Irma Karen klopez@cecs.cl

LUCAR Olivier olivier.lucar@gmail.com

MARINELLI Ludovica ludo.marinelli@gmail.com

MARTIN-GALLAUSIAUX Camille cmartingallausiaux@gmail.com

MIKHAILOVA Anastasia anastassia.mikhailova@pasteur.fr

OUHACHI Melissa melissa.ouhachi@gmail.com

PECKEU Laurène l.peckeu.mcj@gmail.com

ROUILLE Thomas thomas.rouille@gmail.com

SAGET Sarah sarah2611@wanadoo.fr

SBIHI Zineb sb.zineb@gmail.com

SEISEN Thomas thomas.seisen@gmail.com

SIMONNET Emilie emilie.simonnet@college-de-france.fr

emilie.jeanne.simonnet@gmail.com

SIQUEIROS Lourdes lsiqueiros@cinvestav.mx

STERLIN Delphine sterlindelphine@gmail.com

TORRES LAZO Victor Renato vicrenatorres@gmail.com

VALLOT Antoine antoine.vallot@etu.upmc.fr

VAN EEGHER Sandy sandy.vaneegher@gmail.com

ZABLOCKI Laurent laurent.zablocki@curie.fr

ZAOUI Maurice maurice.zaoui1@gmail.com

ZHANG Xufei xufei_zhang@yahoo.com

xufei.zhang@jouy.inra.fr

ZHOU Xianlong anata_79677162@qq.com

3rd YEAR PhD student

BEUTIER Héloise heloise.beutier@pasteur.fr

helob16@hotmail.com

BATAILLE Aurélien aurelbataille@gmail.com

BOITARD Solène solene.boitard@gmail.com

BOUYGUES Anaïs bouygues.anais@gmail.com

DE SETA Daniele daniele_deseta@yahoo.it

DELIGNAT Sandrine sandrine.delignat@crc.jussieu.fr

EYMARD Florent eymard.flo@gmail.com

FADLALLAH Jehane jehane_fad@yahoo.fr

FLOREZ CORREDOR Laura Maria lauraflorez@gmail.fr

GALL Julie julie.gall@sfr.fr

GEA-MALLORQUI Ester ester.gea@curie.fr

GENSER Laurent laurent.genser@gmail.com

GEORGE Caroline caroline.george@inserm.fr

GRANJON David dgranjon@ymail.com

HAMMOUDI Nadjib nadhammoudi@yahoo.fr

HANBOUCH Linda linda.hanbouch@gmail.com

HANOUNA Guillaume gui.hanouna@gmail.com

HIRSCH Pierre hirschpierre@gmail.com

ING Mathieu mathieu.ing@hotmail.fr

mathieu.ing@crc.jussieu.fr

JAILLET Cyprien jailletcyprien@gmail.com

JEZIOROWSKA Dorota d.jeziorowska@fondation-ican.com

LANDMAN Cécilia cec.landman@gmail.com

LE MOIGNIC Aline a.lemoignic@yahoo.fr

LEVIN Clément clement.levin@gmail.com

LI Wu Zhi zhi.li@pasteur.fr

LIU Jin liujin1986413@gmail.com

LIU Yuanhui liuyuanhui10@hotmail.com

LOEUILLARD Emilien loeuillard_e@hotmail.fr

LOISEAU Camille camille.loiseau1@etu.upmc.fr

camille-loiseau@live.fr

LUNELLI Luca luca.lunelli@gmail.com

LUQUE Yosu yosu.luque@gmail.com

MASSARWEH Ahmad ahmadmassarwa@yahoo.com

MESDOM Pierre mesdompierre@hotmail.f

MICELLI-LUPINACCI Renato rmlupinacci@gmail.com

MONSEL Antoine antoine.monsel@gmail.com

MONTASSAR Fadoua fadoua.montassar@gmail.com

MUNTEANU Mona mona.munteanu@biopredictive.com

NABULSI QOSSQOSSI Maisa maysanabulsy@yahoo.com

NEFLA Meriam meriam.nefla@gmail.com

NICOLAS Anthony nicolas_anthony@hotmail.com

QUENTIN Emily emily.quentin@inserm.fr

azegaga@gmail.com

QUINIOU Valentin valentin.quiniou@gmail.com

RAGOT Hélène helene.ragot@gmail.com

RENARD PENNA Raphaele raphaele.renardpenna@gmail.com

ROCHEFORT Juliette julietterochefort@yahoo.fr

RONIN Emilie ronin.emilie@hotmail.fr

ROSENBAUM David davidrosenbaumm@gmail.com

ROUERS Angeline angeliner54@gmail.com

angeline-marie@wanadoo.fr

SALEM Joe-Elie joeelie.salem@gmail.com

SCHMITT Charlotte schmitt.cha@gmail.com

charlotte.schmitt@crc.jussieu.fr

SERBIN Bettina betti.serbin@gmail.com

SONNEVILLE Florence sonneville.florence@gmail.com

SOUSSI Hedi hedi.soussi@hotmail.fr

STEPHEN-VICTOR Emmanuel esvkai@gmail.com

TANNOUS Cynthia cynthiajtannous@gmail.com

TOUCH Sothea sothea.touch2@gmail.com

USUNIER Benoît benoit.usunier@gmail.com

VALLIN Benjamin benjamin.vallin@hotmail.fr

VOISIN Sarah sarahboule@hotmail.com

The Organizing Committee

Cécile BANDET

Marion DAJON

Ray EL BOUSTANY

Sarah GHEZZAL

Annaelle JAROSSAY

Hélène KAPLON

Barbara POSTAL

Elodie PRAMIL

Sami AYARI

Jules RUSSICK