Humeral ImmunityHumeral ImmunityHumeral ImmunityHumeral Immunity

*Ag recognition & presentation:

-APC engulf m.o. , which under go incomplete digestion.- fragmentation of Ag to different epitopes.IL-1- epitipes exposed to the surface of APC (on MHC II ).- so the presentation of epitopes on MHC II

activate T helper.-T helper carries CD4 receptor for MHC II.- T helper stimulate B cell ( which carry BCR ) for produce

plasma cells [ produce Ab ] & memory cell ( prolonged life span ).

this occur through APC..

1ry immune response1ry immune response

*The body exposed to Ag for 1st time.

*plasma cell produced Ab is responsible.

*longer time for Ab production.

*IgM level is predominant.

*the body exposed to Ag for 2nd time.*memory cell is responsible.*shorter.*IgG is predominant ( stronger IR )

Exogenous Ag

APCB cell

T helperActive

B cell

Memory cell Plasma cell

MHC II

TCR

CD4

CD3

APC

Th

Cell mediated immunity

Endogenous Ag

Viral infected cell or intracellular bacterial infected cell

Activate

Activate T

Cytototxicity to

MHC ICD4

CD3TCR

TC CD8 (CDs)

Antibody(immunoglobulin)(Ab)(Ig)

General characters of antibody1-*Ab are group structurally related glycoprotein

that are produced following stimulation of the immune system by immunogen.

2-*Ab.can binds specifically to the Ag molecules. Ab matches Ag much as a key match a lock .4-*Ab found in different type of tissue , but

highest conc. Is found in the blood.5-*they are ∂ globulin& secreted by plasma

cells.

Two identical Light chain

Two identical heavy chain

Antibody structureConsist of four polypeptide, shaped to form .

Ag binding

Light chain

FC*variable protein.

*constant.

FAb

Hinge

Heavy

Ci

VLVL

CBS

Called variable region includes the end of ( VL & VL ) heavy & light chain these unique contours in the Ag binding site.( FAb ) fragment Ag binding.

*the stemof Y shape are constants in all Ab of the same classes ( IgEs ) called ( constant region ) .Compose of Ć complement binding site & cell binding site.The antibody inactivate Ag by: A* Complement fixation. B* Neutralization. C* Agglutination. D* Precepitation .

*tip of Y shape arms vary greatly from Ab to another.

Classes of Antibody ( Ig )

Nine classes..IgG , IgA , IgE , IgD & IgM

Four type 2 type ( subclasses )

(IgG ) Gamma immunoglobulin Monomere ( 75 ) – 75% of serum IgG.

IgG subclasses. IgG 1 , IgG 2 , IgG 3 , IgG 4 .

Differ in no of disulphide bond & length of hinge region.

it is the major Ig in blood .Its mdecular weight is 160,000 .

IgAThere are two types of IgA . the serum Iga which is similar in structure to IgG , and the secretory IgA which is composed of two molecules bound together by a secretory piece and a J chain secretory IgA is found in different body secretions e.g saliva, tears ,milk , colostrums gastrointestinal and respiratory mucous secretions.

It acts as a1st line of defense against invadina bacterial and viruses at

J chain

Secretory

mucous

IgDAs IgG in structure found inserted

into the membrane of B cells.

IgEIs normally present in only trace

amounts but it is responsible for symtoms of allergy.

IgMUsually combines in star –shaped

clusters . it tends to remain in the blood strem . its m.w is 1,000,000 .

It has high binding capacity.

Disulphide bond

J chain

Hypersensitivity

*inappropriate immune response can lead to tissue damage.

*when an individual has been immunologically 2nd boosting of immue response.

*however, the reaction may be excessive & lead to tissue damage ( hyper sensitivity )Or any immune response against foreign Ag that are exaggerated beyond normal.

There are 4 types…

Type I .. hypersensitivity immediate hypersensitivity

Type II .. hypersensitivity cytotoxic hypersensitivity.

Type III .. hypersensitivity immune complex mediate h.

Type IV .. hypersensitivity delayed or cell mediate h.

Type I , II , III mediate by Ab.

Type IV mediated by Tcell.

Type I time 2-3 min

*it is localized or systemic reaction that result from the release of in fl. Molecules in response to Ag .

*it is group of conditions that occur in people a hereditary predisposition to develop IgE against common environmental Ag.

(Ag called allergens) *developed in second or minutes following

exposure to Ag.* it is commonly called allergies.

…Mechanism...

Allergen ) Ag (

1-Ag presenting cell phagocytosis & process Ag .2-APC present Ag determinate to Th2.

3-Th2 produce greated IL4 which stimulate B cell.

4- Bcell become plasma which secret TgE. 5- IgE binds to most cell, basophiles and

eosinophite .

A*sensitivation ( 1,2,3,4,5) 2nd exposure to allergen . stimulate the previous cell to produce histamine , inflammatory molecules serotonin , protease , leukotriene & prostaglandins.

B*degradulation e.g 1- destruction of B.cell following incompatible blood transfusion

2 -destruction of fetal RBC's in heamolytic disease of new born.

Type III 2-8 hrs

Immune complex mediated hypersensitivity.

…mechanism…AG—Ab complex deposited at various site induces most cell degranulation via mast cell , PMN lead to damage of tissue.

Example..Arthus reaction ( localsed)Serum sickness.

Type IVDelayed h. or cell mediate h. time 18-72 hrs.

…mechanism…Memory Th1 release cytokines.Example..

1-Tubercular lesion in Tuberculin Test.2-contact dermatitis.

Clinical signs…Usually localized or mild depend on site of entry

Inhaled Ag hay fever (allergic rhinitis ). Nasal discharge, watery eye, sneezing itching throat & eye.Oral Ag diarrhea.

Skin Ag urticaria , itching.

Example ..

cat hair – penicillin – pollen grain – flowering – plant _bee venom – eggs- peanut – dust mites.

Death due to systemic release of vasoactive mediators general vasodilatation & smooth muscle constriction result in sudden loss of blood pressure , massive edema , severe bronchial constriction ( systemic ).

Type II : cyto toxic sensitivity time 5-8 hrs.

It is damage reaction is caused by specific Ab binding to cells or tissue Ag.

Often due to combined activities of Ć & Ab binding to phagocytes or by ADCC ( K cell ).

Systemic anaphylaxis.