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Lecture 2

Immunoglobulin


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Objectives;
Define       secretary IgA
Describe  structure & functions of IgM
Compare  the antigenic receptor of B 

lymphocyte

Assess     the role of IgE in Atopy
Distinguish  between Isotype, Allotype &    

Idiotype 

Explain     Anti-idiotype Ab
List           the characteristic of specific    

Immune response 

Compare  between primary &        

secondary Immune Response


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IgA

Constitute 15% of total serum Ig

Main Ig in 

the external secretions 

as saliva 

tears breast milk

Subdivided into IgA1 & IgA2 subclasses

It has 2 forms ;

1-Monomeric in the blood 

2- dimeric in the external secretions  


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Dimeric IgA 

• IgA synthesized by plasma cell as monomeric  

one in the submucosa which will be combine 
with another monomeric IgA by a 
polypeptide  J  chain to form dimeric IgA this 
will be protected by a secretary piece from 
the secretary epithelium to form the 

secretary IgA 


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Secretory piece(

SP

):

. Produced by

mucosa epithelial cells

.  

Secretory IgA (sIgA)

.  Functions: 

protect sIgA, resist        proteolysis in 

extra secretory liquid.

IgA

J chain

SP


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IgA

1. Two types  

Serum type

monomer

Secretary type(sIgA)

: dimer

2. Two subclassesIgA1IgA2


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Functions of secretary IgA

Activation of the complement 

through the alternative pathway

Blocking & Neutrilization
opsonization


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IgM

• Constitute 10% of total serum Ig
• Its molecular weight 900 000 (

Heavy

)

• It has 2 forms

1-Monomeric form on the surface of 

B    

lymphocytes as antigen Receptor

together   with IgD

2-

pentameri

c IgM    5 monomeric connected   

by J chain 


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Pentameric IgM


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• IgM has no hinge region replaced by an 

additional domiain(CH2)---CH3,CH4

• Pentameric IgM has 10 FAB so it is the most 

agglutinating & complement fixing Ab 

• It is the main Ig in the primary immune 

response

• It is the 1

st

Ig synthetized by the fetus  


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IgD

Very low concentration in the blood less 
than 1%
Short half life 2-3 days
Present on the surface of B lymphocyte 
together with monomeric IgM as a 

surface 

antigen receptor of B lymphocyte

Immature B cell only IgM on its surface 

Mature B cell IgM+IgD on its 

surface


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IgD


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IgE

• 0.002 % of serum Ig ( detection by Elisa)
• In atopic patient the level increase by 

handreds

• IgE also called 

Reagenic or homocytotropic Ab 

because of its ability  of binding to FC 
receptors on the surface of 

Mast cells

basophiles


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Fc

e

RI

degranulation 

IgE

allergen

inflammation


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Functions of IgE

• Triggering an acute inflammatory reaction

• Has the ability to bind to FC receptor on 

eosinophils so 

important against parasitic 

infections 

eosinophils contain granules that realize cat 

Ionic proteins which are toxic to the parasites 


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IgE increases in 

• Parasitic infections 
• Atopic patients

IL 4 causes switching of Ig to IgE

IL 5 causes eosinophilia 


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Fc

e

RI

degranulation 

IgE

allergen

inflammation


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Variants of Ig

• Isotype

all classes ,Subclasses & forms of Ig 

which present in normal individual 

• Allotype

existence of allelic forms , single a.a. 

variation in the peptide chain of Ig ( genetic 
marker) IgG =GM,  IgA=AM

• Idiotype

each Ig has its own antigenic 

determinant area against which an anti-
idiotype Ab will be formed (Idiotype  

antiidiotype network) 


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A.I.  vaccine

Anti idiotype vaccine

Anti idiotype vaccine


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Anti idiotype vaccine


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Characteristics of sp. Immune respond :

1-Discrimination (distinguish) between self &
Foreign Ag

Any Ag when reach the lymphoid tissue during 

pre-natal period           suppress any further 
immunological response to that Ag in future 
((self))

_

colonel deletion theory 

_

During embryonic dev. All T & B lymphocytes that 

carry auto –reactive receptors for  self Ag            
(       (  

Auto-reactive cells

) will be deleted by               

apoptosis            

self tolerance


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2- specificity

Ab react specifically with Ag that  causes its 

production ,sometimes can react with similar 
not identical = cross reaction

β- haemolytic streptococci can lead to 

rheumatic heart dis

. Because cross reaction 

between bacteria Ag & valve tissue in some 
individuals   


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3-clonality 

We have more that  10   T & B lymphocytic   

clones (group) each clone with different Ag 
receptor, when the Ag enter the body  
lymphocytes bearing receptors that fit the 
epitope best are stimulated to divided                        

(clonal selection theory) 

this response is 

called 

primary immune response 

8


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Clonal Selection of B Cells is Caused by 

Antigenic Stimulation


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B lymphocyte development (2)


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4-Anamnest response :(memory)

The primary I.R. (1

st

exposure)

a-Lag phase (7days) Ab level is zero (time for 

finding appropriate Ag receptor) depend on 
nature ,routs, immune state 

b-Log phase Ab(mainly IgM) start to appear & 

increase logarythemly 

c-Plateau phase 
d-decline phase 


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Secondary I.R. (2

nd

exposure) 

there is 

memory

cell so no lag 

phase ,Ab titer quickly shooting 

up 10-100 times 

*There is genetic switching from 

IgM in the pri. I.R. to 

IgG

in the 

2

nd

I.R. 


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Primary I.R.

Secondary I.R.

* There is lag phase

*No lag phase

*IgM class

*Ab of IgG class

*Low affinity Ab

*Ab of high affinity 

*Ab titer is low 

*Ab titer is high 

*The host exposure for the 
1

st

time so no memory cell

*Host exposure for the 2

nd

time there is memory cell

*Ab titer decline rapidly

*Ab titer decline slowly 


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Best example is the 

vaccination

we 

give booster 

Doses(multiple doses) to shift the I.R. 
from primary to secondary I.R.


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THANK YOU




رفعت المحاضرة من قبل: Abdalmalik Abdullateef
المشاهدات: لقد قام 15 عضواً و 218 زائراً بقراءة هذه المحاضرة








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