Download Cell media

Humeral immunity
*Ag recognition & presentation:
this occur through APC..
-APC engulf m.o. , which under go incomplete digestion.
- fragmentation of Ag to different epitopes.
- epitipes exposed to the surface of APC (on MHC II ).
- so the presentation of epitopes on MHC II
IL-1
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 ).
1ry immune response
1ry 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
B cell
APC
APC
Active B cell
Memory cell
T helper
MHC II
Plasma cell
TCR
CD4
CD3
1
Th
Cell mediated immunity
Endogenous Ag
Viral infected cell or
intracellular bacterial
infected cell
MHC I
CD4
CD3
TCR
Activate Th
Tc
Activate T cytotoxic
CD8
(CD8 cell)
Cytototxicity to Ag
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.
-3Ab 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.
2
Antibody structure
Consist of four polypeptide, shaped to form.
Two identical
heavy chain
Two identical
Light chain
Ag binding site
VL
VL
Light chain
chain
FAb
FC
Heavy chain
*variable protein.
*constant.
C
i
Hinge region
C
B
S
Heavy chain
*tip of Y shape arms vary greatly from Ab to another .
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.
3
Classes of Antibody ( Ig )
Nine classes..
IgG
,
Four type
IgA
,
IgE
,
IgD & IgM
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 mucous
Secretory piece
J chain
4
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
5
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
Type IV
mediate by Ab.
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.
6
…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.
7
Type IV
Delayed 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.
Systemic anaphylaxis .
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 ).
Fine…
8