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immunology
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IMMUNOPATHOLOGYHYPERSENSITIVITY
BY GOMATHI.M
IMMUNOPATHOLOGY
0Defects or malfunction in either innate or acquired immune response provokes the illness or disease.
0Overactive immune response-Hypersensitivity0 Inappropriate reaction to self-autoimmunity0 Ineffective immune response-immunodeficiency
HYPERSENSITIVITY
0Undesired immune response
0Hypersensitivity is a state existing in a previously sensitized individual which leads to tissue damage on later exposure to the allergen.
0 It depends on the individual.
HISTORY02000 years ago, Lucretius states that “Differences are so
great that one man’s meat is another man’s poison”.
0Paul Poiter and Charles Richet- Pysalia the jelly fish- aqueous glycine extract administered to 5 dogs but they didn’t die. But after the second dose immediately reacted with illness, vomiting, diarrhea, asphyxia and died within few minutes.
0Hence they coined this overreaction as anaphylaxis.0Awarded Noble Prize in physiology or medicine in 1913 .
01st exposure-sensitization02nd exposure- shocking dose 0Anaphylaxis- without protection rather than an
anamnestic (non forgetting) protective response.
0Anaphylaxis :0 humoral immunity – immediate hypersensitivity0Cell- mediated immunity – delayed-type hypersensitivity.
CAUSES OF HP DISEASES
0Reaction against environmental antigens – production of IgE antibodies cause allergic reactions.
0Reaction against microbes
0Autoimmunity
CLASSIFICATION OF HYPERSENSITIVITY
0 In 1960s Gell and Coombs classified it into 4 types .
0Type I – Immediate anaphylaxis 0Type II – antibody – dependent cytotoxic hypersensitivity0Type III – Immune complex-mediated cytotoxicity0Type IV – delayed type hypersensitivity
TYPE I HYPERSENSITIVITY0CHARACTERISTICS: 0occur quickly after 2nd exposure to the antigen or allergen 0 Inflammation reaction consists of accumulation of basophils,
eosinophils, neutrophils, Th2 cells0 IgE mediated response0Antigens – plants, foods, drugs, insect products, mold
spores, animal hair, foreign serum, vaccines0Atopy : the genetic predisposition to synthesize
inappropriate levels of IgE specific for external allergens
MECHANISM
Slow reacting substance of anaphylaxis
Degranulate and release the biological mediators
Preformed granule mediators New generated mediators
Histamine Bradykinin Leukotrienes Platelet activating factor Prostaglandin D2
Dilate capillaries,increase permeability, increase mucus secretion, contract smooth muscle
Systemic anaphylaxis Skin Respiratory tract Degist tract
Drug therapy: sodium chromoglcate-stabilize PM & inhibit degranulation
Antihistamine & acetyl salicylic acid
Treat target organs
TYPE II HYPERSENSITIVITY0CHARACTERISTICS:
0Antibody dependent cell-mediated cytotoxicity (ADCC)
0Antibody (IgM & IgG) activate the complement system which lyse the cell and destroy it.
MECHANISM
Allergen
Stimulate
Antibody
A. Opsonic phagocytosis
D. ADCC of NK
C. Effect of complement
Combined opsonic activities
Cell injury ways of type II hypersensitivity
Cell
Antigen or hapten on cell
Antibody (IgG, IgM)
Activate complement
Lyse target cell
Opsonic phagocytosis NK , phagocyte Stimulate / block
Destroy target cell ADCC
Target cell injury Change the function ofTarget cell
Mechanism of Type II hypersensitivity
DISEASES
0TRANSFUSION SYNDROME
0ERYTHROBLASTOSIS FOETALIS
0DRUG INDUCED AUTO HEMOLYTIC ANEMIA
TYPE III
Free Ag + Primed Ab Larger immune complex
Deposit in tissue or blood vessel wall
Inflammation
TYPE III
2 、 Mechanism of type III hypersensitivity
Formation of the intermediate immune complex
Deposition of the intermediate immune complex
Tissue injury by the immune complex
Soluble antigen Body Antibody
Immune complex
Small molecular soluble Immune complex
intermediate molecular soluble Immune complex
Large molecular insoluble Immune complex
Deposit on the basement of capillaries
Combine and activate complement system
C3a,C5a,C3b
Infiltration of neutrophils
Phagocytose complex
Release the enzymes in lysosome
Tissue injury
Eliminate by phogacytosis
Platelets
Thrombus
Aggregation of platlets
Blood Clotting MechanismsRelease of vasoactive amine
Increase vascular permeability
Bleeding Edema
Basophils and mast cells
Release of vasoactive amine
Increase vascular permeability
Edema
Local or systemic immune complex diseases
3. common disease of type III hypersensitivity 1. Local immune complex disease
Arthus reaction : Experimental local reaction, Necrotic vasculitis vasculitis, Ulcer
Human local reaction: insulin-dependent diabetes mellitus (IDDM) 2. Acute systemic immune complex disease
serum sickness Anti-serum Ab+Ag systemic tissue injury ,fever, arthritis, skin rash Pinicillin、 Sulfanilamide
Acute immune complex glomerulonephritis : Streptococcus infection
3. Chronic immune complex disease
SLE Rheumatoid arthritis : RF+IgG Deposit on synovial membrane
5. Type IV hypersensitivity
1 、 characteristics of type IV hepersensitivity
2 、 mechanism of type IV hepersensitivity
3 、 common diseases of type IV hepersensitivity
1. Characteristics
Interaction of primed T cells and associated antigen
Infiltration of Mononuclear Cells, Inflammatory response
2. Mechanism of type IV hypersensitivity
Formation of effector and memory T cells
Inflammation and cytotoxicity caused by effector T cells
1) Inflammation and tissue injury mediated by CD4+Th1
Release chemokines and cytokines
Immune injury mainly caused by infiltration of mononuclear cells and
lymphocytes
2) Cytotoxicity of CD8+CTL
Antigen T cell(CD4+,CD8+)
Secondary contact
Induce
Primed T cell
CD4+ T cell
CD8+ T cell
ReleaseCytokines
IL-2TNF-bINF-g
TFMCFMIFMAFSRF
Directly kill target cells
Infiltration of monocyte and Mf
Proliferation of T cell
Exudation and edema
Cytotoxicity
Inflammation characterized by infiltration of Mf , monocyte, And tissue injury
Mechanism of type IV hypersensitivity
3. Common disease of type IV hypersensitivity
1) Infectious delayed type hypersensitivity
OT( Old Tuberculin ) test
2) Contact dermatitis :
Paint, drug red rash, papula, water blister, dermatitis
3) Acute rejection of allogenic transplantation and
immune response in local tumor mass
Same disease (SLE), multiple immune injury ,hypersensitivity involved
Same drug (penicillin), several types of hypersensitivity
SUMMERY
THANK YOU……..
0 Immunopathology, diagnosis, and management of hypersensitivity pneumonitis.0 Abstract0 Hypersensitivity pneumonitis (HP) is an inflammatory interstitial lung disease caused by a wide variety of organic
particles and certain small-molecular weight chemical compounds that provoke an exaggerated immune response in susceptible individuals. The clinical manifestations are heterogeneous and have been classically described as acute, subacute and chronic. The chronic form has an insidious onset over a period of months or years, with progressive dyspnea and often evolves to fibrosis. The pathology is characterized by a bronchiolocentric interstitial mononuclear cell infiltration, nonnecrotizing poorly formed granulomas, cellular pneumonitis and variable degrees of fibrosis. However, morphological diagnosis of HP is complicated because the subacute/chronic forms may be difficult to distinguish from idiopathic pulmonary fibrosis/usual interstitial pneumonia and nonspecific interstitial pneumonia. In general, diagnosis of HP represents a challenge for clinicians that need to weigh a constellation of clinical, laboratory, radiographic and (when available) pathological evidence for each patient to assess the certainty of the diagnosis. The cornerstone of therapy is antigen avoidance. Although clinical trials are scanty, corticosteroids are usually indicated based upon expert opinion. In this review we summarize the current evidence regarding the diagnostic criteria and therapeutic strategies as well as the immunopathological mechanisms putatively implicated in the development of the disease.
0 Arch Pathol Lab Med. 2008 Feb;132(2):204-5. doi: 10.1043/1543-2165(2008)132[204:HPAIR]2.0.CO;2.0 Hypersensitivity pneumonitis: an immunopathology review.0 Woda BA.0 Source0 Department of Pathology, University of Massachusetts Medical School, Worcester, USA. [email protected]