Humeral 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 response *the body exposed to Ag for 2 nd time. *memory cell is responsible. *shorter. *IgG is predominant ( stronger IR ) *The body exposed to Ag for 1 st time. *plasma cell produced Ab is responsible. *longer time for Ab production. *IgM level is predominant.

Exogenous Ag APCB cell T helper Active 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 I CD4 CD3 TCR TCCD8 (CDs)

Antibody(immunoglobulin) (Ab) (Ig) General characters of antibody 1-*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 structure Consist of four polypeptide, shaped to form. Ag binding Light chain FC *variable protein. *constant. FAb Hinge Heavy CiCi VL CBSCBS

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.

IgA There 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

IgD As IgG in structure found inserted into the membrane of B cells. IgE Is normally present in only trace amounts but it is responsible for symtoms of allergy. IgM Usually 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 IV Delayed h. or cell mediate h. time 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.