Lecture Nr. 6, Immunity, 16.03.11

8/2/2019 Lecture Nr. 6, Immunity, 16.03.11

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Summaryof previous lesson

Macrophage Attacking E.coli (SEM x8,800) Dr Dennis

KunkelAlveolar (Lung) Macrophage Attacking E. coli (SEMx10,000) Dr Dennis Kunkel (used with permission)


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Horton & Parker: Informed Infection Control Practice

I. Chain of Infection


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HOST DEFENSE

MECHANISMS


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Lecture nr. 6

Antigens. Antibodies.Immune response.

Cell cooperation and

mediators in immune

response.

15.03.2011


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HOST DEFENSE

MECHANISMS


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Immunity: Free from burden. Ability of anorganism to recognize and defend itself againstspecific pathogens or antigens.

Immunity refers to the ability of the human body toresist disease agents and their toxins throughpossession of antibodies.

Immunity is a long lasting protection against a

specific antigen.

Definitions of theImmunity


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Specific Host Defenses:The Immune Response

The structure of immunoglobulinsT-cell (part of the specificimmune response)


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The ImmuneResponse

Immune Response: Third line of defense.

Involves production of antibodies and

generation of specialized lymphocytes

against specific antigens.

Antigen: Molecules from a pathogen or

foreign organism that provoke a specific

immune response.


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What is the immune

system?

The bodys defense against disease causing

organisms, malfunctioning cells, and foreign

particles


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Microbes are recognized by two mechanisms: evolved broad recognition mechanisms (innate

immunity), and by highly specific lymphocyte antibodies and T cell

receptors (adaptive immunity)

Different types of microbes are eliminated bydifferent effectors mechanisms, which aredesigned to best combat each type of microbe

How does the immune system

respond to different infections?


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Classification

of immunity


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Classification

of the immunity


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A. Naturally Acquired Active Immunity: Antigens or pathogens enter body naturally.

Body generates an immune response to antigens.

Immunity may be lifelong (chickenpox or mumps) or temporary(influenza or intestinal infections).

B. Naturally Acquired Passive Immunity: Antibodies pass from mother to fetus via placenta or breast feeding

(colostrum). No immune response to antigens.

Immunity is usually short-lived (weeks to months).

Protection until childs immune system develops.

Acquired Immunity:Obtained in the course ofdaily life.


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Classification

of the immunity


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Beneficial:

Protection from Invaders

Elimination of Altered Self

Detrimental:

Discomfort (inflammation)

Damage to self (autoimmunity)

Significance of the

Immune System


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Components of HumanImmune System


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Cells of the immune system

Lymphocytes Mediators of adaptive immune responses; only cells with

specific receptors for antigens

Antigen-presenting cells (APCs) Specialized to capture, concentrate, and display antigens for

recognition by lymphocytes Dendritic cells; macrophages, B cells; follicular dendritic

cells Different APCs serve different roles in adaptive immune

responses Effector cells

Function to eliminate microbes; include lymphocytes,granulocytes (neutrophils, eosinophils), macrophages


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To become mature, immunocompetent cells, they must

pass through lymphoid tissues in other parts of the

body.As they do so, they become committed to becoming

eitherT cells or B cells1. Cells that migrate through the bone marrow (bursalequivalent) become B cells , and will produce antigensand

participate in humoral immunity.

2. Cells that migrate through the thymus glandsbecome T cells and participate in Cell-mediated

Lymphocytes


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Congenital immunodeficiency diseases are often caused by blocksat different stages of lymphocyte maturation

LYMPHOCYTE DEVELOPMENT


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CD Nomenclature

Structurally defined leukocyte surface molecule thatis expressed on cells of a particular lineage(differentiation) and recognized by a group(cluster) of monoclonal antibodies is called a

member of a cluster of differentiation (CD) CD molecules (CD antigens, CD markers) are: Identified by numbers Used to classify leukocytes into functionally distinct

subpopulations, e.g. helper T cells are CD4+CD8-, CTLs areCD8+CD4-

Often involved in leukocyte functions

Antibodies against various CD molecules are used to: Identify and isolate leukocyte subpopulations Study functions of leukocytes Eliminate particular cell populations


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Two types of T cells: coordination of

function with properties of antigen-

presentation

CD4 T cells

.Help other immune cells

Recognize peptide + MHC

II

MHC II is expressedprimarily on immune

cells

Peptides are from

endoc tosed anti en

CD8 T cells

.Kill virus-infected cells

Recognize peptide + MHC

I

MHC I is expressed on

all nucleated cells

Peptides are fromc tosolic anti en


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ANTIGENS


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An antigen is a molecule that stimulates an immune

response.

The word originated from the notion that they can

stimulate antibody generation.

The modern definition includes all substances that can be

recognized by the adaptive immune system.

Antigens


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Chemical nature of

antigen

Proteins

Polysaccharides

Nucleic acids

Lipids Some glycolipids and phospholipids can be

immunogenic for T cells and illicit a cell-mediated immune response


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Most are proteins or large polysaccharides from a

foreign organism. Microbes: Capsules, cell walls, toxins, viral capsids, flagella, etc.

Nonmicrobes: Pollen, egg white , red blood cell surfacemolecules, serum proteins, and surface molecules from

transplanted tissue.

Lipids and nucleic acids are only antigenic when combined

with proteins or polysaccharides.

Molecular weight of 10,000 or higher.

Antigens


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Antigens can be classified in

order of their origins

Exogenous antigens - are antigens that have

entered the body from the outside, ex. by inhalation, ingestion, or injection.

By endocytosis or phagocytosis, these antigens are taken into the

antigen-presenting cells (APCs) and processed into fragments.

Endogenous antigens - antigens that havebeen generated within the cell, as a result

of: normal cell metabolism, or


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Allogenic antigen

The specific antigen exists in different individuals.

Blood type antigens.

Autoantigensusually a normal protein (sometimes DNA or RNA) that is

recognized by the immune system of patients sufferingfrom a specific autoimmune disease.

Types of Antigens


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Self Antigens Antigens of our own cells

Do not cause an immune response in our

body Usually cause an immune response in another

person

MHC proteins Major Histocompatibility Complex


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are presented by the MHC I molecules on the surface of

tumor cells. can sometimes be presented only by tumor cells and

never by the normal ones.

they are called tumor-specific antigens (TSAs) andtypically result from a tumor specific mutation.

Tumor antigens


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Characteristics of

AntigenImmunogenicity

The capacity to stimulate the production of

antibodies or cell-mediated immune

responses.


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Antigenicity

The ability to bind antibody.

Complete antigen

Incomplete antigen, also known as

hapten.

Hapten: Small foreign molecule that is not antigenic. Must be coupled to a

carrier molecule to be antigenic. Once antibodies are formed they will

recognize hapten.

Characteristics of

Antigen


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Epitope or, Antigenic determinants:

Small part of an antigen that interacts with an

antibody. Any given antigen may have several epitopes.

Each epitope is recognized by a different

antibody and may interact with them by

paratopes ofAntibody

Antigens

F

e


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Epitopes: Antigen Regions that Interactwith paratopes, Antibodies regions


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Types of Epitopes1. Linear epitopes

continuous and found in polysaccharides

as well as in both native (nondenatured) anddenatured proteins, especially fibrillar

proteins.

specificity depends upon primary

sequence.

typical size is 5-6 subunits in length.


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2. Conformational epitopes Discontinuous (involve multiple subunits,

often located far apart in the primary

sequence of the antigen molecule) and are

thus found only in native (globular)proteins.

Types of Epitopes


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Antigenic epitopes


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Two differentepitopes

B cell epitope, a portion

of antigen molecule thatis recognized by B cell

receptors.

T cell epitope, the

region of antigenmolecules that are

recognized by T cell

receptors.


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Antigens: T-independent

Activate B cells without MHCclass II T help

Polysaccharides Properties Polymeric structure Polyclonal B cell activation, but poor

memory Resistance to degradation

Examples Pneumococcal polysaccharide, LPS Flagella


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Antigens: T-dependent

Require T help to activate B

cells

Proteins Examples

Microbial proteins

Non-self or altered-self

proteins


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Hapten-carrier

conjugates Definition

Ag only if bound to carrier protein

Structure Native determinants

Haptenic determinants


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ANTIBODY


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Proteins that recognize and bind to a particular antigenwith very high specificity.

Made in response to exposure to the antigen.

One virus or microbe may have several antigenicdeterminant sites, to which different antibodies may bind.

Each antibody has at least two identical sites that bindantigen: Antigen binding sites.

Valence of an antibody: Number of antigen binding sites.Most are bivalent.

Belong to a group of serum proteins called

immunoglobulins (Igs).

Antibodies


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Monomer: A flexible Y-shaped molecule with fourprotein chains:

2 identical lightchains 2 identical heavy chains

Variable Regions: Two sections at the end of Ys arms.Contain the antigen binding sites (Fab). Identical onthe same antibody, but vary from one antibody toanother.

Constant Regions: Stem of monomer and lower parts ofY arms.

Fc region: Stem of monomer only. Important becausethey can bind to complement or cells.

AntibodyStructure


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Immunoglobulins

IgG - monomer

IgA dimer 2 units

IgM pentamer 5 units IgD monomer

IgE monomer


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Structure: Monomer

Percentage serum antibodies: 80%

Location: Blood, lymph, intestine

Half-life in serum: 23 days

Complement Fixation: Yes

Placental Transfer: Yes

Known Functions: Enhances phagocytosis, neutralizes

toxins and viruses, protects fetus and newborn.

I. IgG


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Structure: Pentamer

Percentage serum antibodies: 5-10%

Location: Blood, lymph, B cell surface (monomer)

Half-life in serum: 5 days Complement Fixation: Yes

Placental Transfer: No

Known Functions: First antibodies produced during an

infection. Effective against microbes and agglutinating

antigens.

II. IgM


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Structure: Dimer

Percentage serum antibodies: 10-15%

Location: Secretions (tears, saliva, intestine, milk), bloodand lymph.

Half-life in serum: 6 days

Complement Fixation: No


Known Functions: Localized protection ofmucosalsurfaceProvides immunity to infant digestive tract.

III. IgA


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Structure: Monomer

Percentage serum antibodies: 0.2%

Location: B-cell surface, blood, and lymph Half-life in serum: 3 days



Known Functions: In serum function is unknown. On B ce

surface, initiate immune response.

IV. IgD


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Structure: Monomer

Percentage serum antibodies: 0.002%

Location: Bound to mast cells and basophils throughout

body. Blood. Half-life in serum: 2 days



Known Functions: Allergic reactions. Possibly lysis ofworms.

V. IgE

Antibodies are Produced by B Lymphocytes


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y y p y


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B cells develop from stem cells in the bone marrow of

adults (liver of fetuses).

After maturation B cells migrate to lymphoid organs(lymph node or spleen).

Clonal Selection: When a B cell encounters an antigen it

recognizes, it is stimulated and divides into many clones

called plasma cells, which actively secrete antibodies.

Each B cell produces antibodies that will recognize only

one antigenic determinant.

Secretions theAntibodies by B cells

Clonal Selection of B Cells is Caused by


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yAntigenic Stimulation


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Programmed cell death (Falling away). Human body makes 100 million lymphocytes

every day. If an equivalent number doesnt die,

will develop leukemia.

B cells that do not encounter stimulating antigen

will self-destruct and send signals to phagocytes

to dispose of their remains.

Many virus infected cells will undergo apoptosis,

to help prevent spread of the infection.

Apoptosis


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Immune response


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Involves production of antibodies against foreign antigens.

Antibodies are produced by a subset of lymphocytes called B

cells.

B cells that are stimulated will actively secrete antibodies andare called plasma cells.

Antibodies are found in extracellular fluids (blood plasma,

lymph, mucus, etc.) and the surface of B cells.

Defense against bacteria, bacterial toxins, and viruses that

circulate freely in body fluids, before they enter cells. Also cause certain reactions against transplanted tissue.

I. Humoral (Antibody-Mediated) Immunity


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Plasma cells secrete antibodies, which can circulate andinteract with antigen.

Antigens are processed by antigen-presentingcells (lots in lymphoid tissues)- macrophages- dendritic cells

- B cells.MHC plays a critical role in antigenpresentation

Humoral Immunity


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How do antibodies actually

help eliminate antigens?


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Antigen-Antibody Complex: Formed whenan antibody binds to an antigen it

recognizes.Affinity: A measure of binding strength.1. Agglutination: Antibodies cause antigens

(microbes) to clump together. IgM (decavalent) is more effective that IgG

(bivalent). Hemagglutination: Agglutination of red blood cells.

Used to determine ABO blood types and to detectinfluenza and measles viruses.

Consequences ofAntigen-AntibodyBinding


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2. Opsonization: Antigen (microbe) is covered

with antibodies that enhances its ingestion

and lysis by phagocytic cells.

3. Neutralization: IgG inactivates viruses by

binding to their surface and neutralize toxins

by blocking their active sites.


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Antibody-dependent cell-mediated cytotoxicity:

Used to destroy large organisms (e.g.: worms).

Target organism is coated with antibodies and

bombarded with chemicals from nonspecific

immune cells.

5. Complement Activation: Both IgG and IgM

trigger the complement system which results in

cell lysis and inflammation.


Consequences of Antibody Binding


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Consequences of Antibody Binding


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Primary Response:

After initialexposure to antigen, no antibodies are

found in serum for several days. A gradual increase in titer, first of IgM and then

of IgG is observed.

Most B cells become plasma cells, but some B cells

become long living memory cells. Gradual decline of antibodies follows.

Immunological responce


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Subsequent exposure to the same antigen

displays a faster and more intense antibody

response.

Increased antibody response is due to theexistence of memory cells, which rapidly produce

plasma cells upon antigen stimulation.

Antibody Titer: The amount of antibody in theserum.

Secondary Response:


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Duality of ImmuneSystem Humoral (Antibody-

Mediated) Immunity

II. Cellular (CellMediated) Immunity


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Involves specialized set of lymphocytes called T cellsthat recognize foreign antigens on the surface of cells,organisms, or tissues:

Helper T cells

Cytotoxic T cells

T cells regulate proliferation and activity of other cellsof the immune system: B cells, macrophages,neutrophils, etc.

Defense against: Bacteria and viruses that are inside host cells and are inaccessible to

antibodies. Fungi, protozoa, and helminths Cancer cells Transplanted tissue

II. Cellular (CellMediated) Immunity


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T cells regulate the immune response

Helper T cells secrete cytokines that regulate the immune

response

IL-2 - induce proliferation of T cellsIL-4, IL-5, IL-6 - activate B cells (and T cells)-interferon - T cell activation

IL-1 is secreted by macrophages; this helps activate Tcells also

Macrophages present antigen to T cells

Cellular Immunity


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Matures inbone marrowthymusType of immunityhumoralcell-mediatedSecretesantibodiescytokinesAntigen receptorsurface IgT cell receptorWhere foundspleenblood, lymph

nodesTargetsbacteria, infected cellsvirusestumor cells?Memory?YesYes

B and T cells mediatespecific immunity

B cells T cells


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Antigens that stimulate this response are mainly

intracellular.Requires constant presence of antigen to remain effective.

Unlike humoral immunity, cell mediated immunity is nottransferred to the fetus.

Cytokines: Chemical messengers of immune cells.

Over 100 have been identified.

Stimulate and/or regulate immune responses. Interleukins: Communication between WBCs. Interferons: Protect against viral infections.

Chemokines: Attract WBCs to infected areas.

T Cells and CellMediated Immunity


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Cellular Components of Immunity: T cells are key cellular component of immunity.

T cells have an antigen receptor that recognizes

and reacts to a specific antigen (T cell receptor).

T cell receptor only recognize antigens combined

with major histocompatability (MHC) proteins on

the surface of cells. MHC Class I: Found on all cells.

MHC Class II: Found on phagocytes.

Clonal selection increases number of T cells.

T Cells and CellMediated Immunity

T Cells Only Recognize Antigen


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T Cells Only Recognize AntigenAssociated with MHC Molecules on Cell

Surfaces


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Types of T cells1. T Helper (TH) Cells: Central role in immune

response. Most are CD4+

Recognize antigen on the surface of antigen presenting

cells (e.g.: macrophage).

Activate macrophages Induce formation of cytotoxic T cells

Stimulate B cells to produce antibodies.

Cells and Cell MediatedImmunity


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Central Role of Helper T Cells


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1. Activated Macrophages: Stimulated phagocytes. Stimulated by ingestion of antigen

Larger and more effective phagocytes. Enhanced ability to eliminate intracellular bacteria, virus-infected

and cancerous cells.

2. Natural Killer (NK) Cells: Lymphocytes that destroy virus infected and tumor cells.

Not specific. Dont require antigen stimulation.

Not phagocytic, but must contact cell in order to lyse it.

Nonspecific CellularComponents


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Cellular Interactions in

the Immune Response


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C ll l I t ti i th


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Cellular Interactions in theImmune Response

Few antigens can activate B cells all by

themselves

For activation of B cells and Tc Cells need asecond signal cytokine ( cell mover)


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Antigen-Presenting cells (macrophages)place antigen on their cell surface in

combination with the MHC II complexAntigen is presented to a specific helper Tcell that has receptors that match theantigen MHC II complex


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Cell surfacepeptides

of Ag


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T and B cells recognise antigen differently

Antigen must be catabolised before T cells can recognise it

Antigen processing generates antigenic peptides

Exogenous antigen processing takes place in lysosomes

Endogenous processing is non-lysosomal

The mechanism of antigen processing depends upon thecompartment in which the pathogen replicates

Endogenous and exogenous antigen processing both involveuptake, degradation, complex formation and presentation

Pathogens can evade immunity by disrupting antigen processing

Summary


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After binding, the APC produces Interleukin-1 (IL-1) which stimulates the TH Cell to

produce IL-2 and/or IL-4Interleukin-2 has an autocrine function,causes TH Cell to clone itself, and make

more IL-2 and /or IL-4


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Helper T cells

TH1 cells produce IL -2 and IFN- and

influence cell-mediated immunity

TH2 cells produce IL -4 (and other ILs)and

influence antibody-mediated (humoral)

immunity


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When B cell comes in contact with theantigen and IL-4, the B cell produces plasmacells and memory cellsTc Cells come in contact with the antigen onthe surface of infected cells in combinationwith the MHC 1 complex. When also have

binding with IL-2, cells produce activated TcCells and memory cells.


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Relationship Between Cell-


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1. Antibody ProductionT-Dependent Antigens:

Antibody production requires assistance from T helper cells.

A macrophage cells ingest antigen and presents it to TH cell. TH cell stimulates B cells specific for antigen to become plasma cells.

Antigens are mainly proteins on viruses, bacteria, foreign red blood cells,

and hapten-carrier molecules.

T-Independent Antigens: Antibody production does not require assistance from T cells.

Antigens are mainly polysaccharides or lipopolysaccharides withrepeating subunits (bacterial capsules).

Weaker immune response than for T-dependent antigens.

Mediated and HumoralImmunity

Humoral Response to T DependentA ti


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Antigens

Humoral Response to T DependentAntigens


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Antigens

Principal mechanisms of defense against microbes


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Antibodies PhagocytesT cells (CTLs)

(may work with antibodies, T cells)

All microbes

All microbes

Intracellularmicrobes, esp.

viruses

Relationship Between


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2. Antibody Dependent Cell Mediated Cytotoxicity Target cell is covered with antibodies, leaving Fc

portion sticking outwards.

Natural killer and other nonspecific cells that have

receptors for Fc region are stimulated to kill targeted

cells.

Target organism is lysed by substances secreted by

attacking cells. Used to destroy large organisms that cannot be

phagocytosed.

Cell-Mediated andHumoral Immunity

Overview of the Immune Response


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Disorders of Immunity


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Hypersensitivity

Exaggerated Immune Response


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Hypersensitivity Types

Allergy Exogenous, non-human antigen

Isoimmunity (alloimmunity) Exogenous, human antigen

Autoimmunity Endogenous antigen


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Type I


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Type I

Immediate hypersensitivity IgE mediated

Exogenous antigen

Most (but not all) Allergies

Type I: Mechanism


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yp

Repeated antigen exposure causes increased IgEproduction

IgE binds to mast cells

Sensitization occurs


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Type I: Signs/Symptoms


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Clinical signs, symptoms = response to histamine

release

GI, skin, respiratory system High mast cells numbers

Most sensitive



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ype S g s/Sy pto s

Histamine effects Vasodilatation

Increased capillary permeability

Non-vascular smooth muscle spasm



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Skin: flushing, itching, edema, urticaria Respiratory: bronchospasm, laryngospasm, laryngeal

edema

Cardiovascular: tachycardia, hypotension

GI: nausea, vomiting, cramping, diarrhea

T I At i


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Type I: Atopia

Allergy prone individuals

Genetic predisposition

More IgE More mast cell receptors for antibodies than

normal


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Type I: Anaphylaxis Severe, generalized Type I reaction

Life-threatening

Loss of airway Ventilatory failure

Hypoperfusion

Type II


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yp

Tissue specific Reaction to tissue-specific antigens

Causes target cell destruction, dysfunction

Exogenous or endogenous antigen

T II


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Type II

Most commonly affected cells Red blood cells

Thyroid cells

Type II: Mechanisms


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Type II: Mechanisms

Antibody binds to cell membrane, triggers

compliment-mediated lysis

Examples Reaction to transfused blood Hemolytic disease of newborn

Type II: Mechanisms


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Type II: Mechanisms

Antibodies promote target cell clearance by

macrophages

Type II: Mechanisms


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Type II: Mechanisms

Antibodies bind to target cells and cytotoxic

T-cells

Trigger release of toxins to destroy targetcells

Type II: Mechanisms


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ype ec a s s

Antibody binds to cell membrane, causes alterations intarget cell function

Example: Graves' disease Antibody binds to thyroid cell membrane

Mimics Thyroid Stimulating Hormone action

Causes production of excessive amounts of thyroid hormone Results in common form of hyperthyroidism

T pe III


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Type III

Mediated by antigen/ antibody complex

deposition in tissues

Exogenous or endogenous antigen

Type III: Mechanism


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yp

Ag-Ab complex deposited in tissues

Especially sensitive tissues are blood vessels, GI,

respiratory system Causes complement activation, increased

neutrophil activity

Neutrophils have trouble digesting complexes,

release lysosomes causing damage

Type III


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yp

Immune complex quantity varies over time Symptomatic periods alternate with periods of

remission

Type III: Serum Sickness


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Type III: Serum Sickness

Repeated intravenous antigen injections

Immune complexes deposited in tissues

Fever, rash, pain, lymphadenopathy

Type III: Raynauds

Phenomenon


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Phenomenon

Temperature governs immune complexdeposition in peripheral circulation

Exposure to cold causes redness, pain of fingers,

toes followed by numbness, cyanosis, gangrene

Type III: Arthus Reaction


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Occurs after repeated LOCAL exposure to

exogenous antigen

Immune complexes in vessel walls

Examples Celiac disease from wheat protein

Hemorrhagic alveolitis from moldy hay inhalation

Type IV


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Delayed

Mediated by Td (lymphokine-producing) or Tc

(cytotoxic) cells

No antibody involved

Type IV


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Examples Graft rejection Contact allergic reactions (poison ivy)

Hypersensitivity Targets


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Hypersensitivity Targets

Allergins Pollen (hay fever)

Drug reactions Foods


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Autoimmune Disease

Clinical disorder produced byimmune response to normal tissue

component of patients body

Graves Disease


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Graves Disease

Antibody stimulates thyroid hormone over

production

Produces hyperthyroidism Antibody, disease can be passed through

placenta

Rheumatoid Arthritis


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Rheumatoid Arthritis

Antibody reaction to collagen in joints

Causes inflammation, destruction of joints

Myasthenia Gravis


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Myasthenia Gravis

Antibodies destroy acetylcholine receptors

on skeletal muscle

Produce episodes of severe weakness Antibodies can cross placenta, affect

newborn

Immune Thrombocytopenic


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Purpura

Antibodies destroy platelets

Produces clotting disorders, hemorrhaging

Antibodies can cross placenta, affectnewborn

Isoimmune Neutropenia


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Isoimmune Neutropenia

Antibodies attack, destroy neutrophils

Can cross placenta, affect newborn

Other Autoimmune Diseases


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Other Autoimmune Diseases

Type I diabetes mellitus

Primary myxedema

Rheumatic fever

Crohns disease

Ulcerative colitis

Systemic Lupus Erythematosis (SLE)


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Immunodeficiency Disease


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Patient unable to fight off infection

Hallmarks

Repeated infections Opportunistic infections



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Most are defects in T cells or B cells T cells, macrophage defects = fungal, viral

infections B cells, complement defects = bacterial

infections



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Congenital

Acquired


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B Cell Deficiency


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B Cell Deficiency

Agammaglobulinemia

Hypogammaglobulinemia

IgA Deficiency


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IgA Deficiency

Most common immune deficiency disorder

Genetic condition

Failure of IgA synthesis Patient has repeated, recurrent sinus, lung, GI

infections

DiGeorges Syndrome


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DiGeorge s Syndrome

Thymic hypoplasia

Severe decrease in T-cell production,

function Defects of face, ears, heart

Severe CombinedI d fi i


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Immunodeficiency

Thymus development arrested at ~6-8 weeks

gestation.

Deficiency, defective maturation of stem cells

that produce B and T cells Little to no antibody production

Acquired


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Acquired

Nutritional deficiency

Iatrogenic (drugs, radiation)

Trauma (prolonged hypoperfusion) Stress

Infection (HIV)

Immune Deficiency Therapies


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Immune Deficiency Therapies

B-cell deficiency: Gamma globulin

SCID: Bone marrow transplants, enzyme

replacement DiGeorges Syndrome: Fetal thymus

transplants

Gene therapy

Documents

Lecture Nr. 6, Immunity, 16.03.11