Transcript IgA

Lecture 2
Immunoglobulin
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
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
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
Secretory piece( SP):
. Produced by mucosa epithelial cells
. Secretory IgA (sIgA)
. Functions: protect sIgA, resist
proteolysis in
extra secretory liquid.
J chain
IgA
SP
Ⅲ. IgA
1. Two types
Serum type ：monomer
Secretary type（sIgA）: dimer
2. Two subclasses：IgA1，IgA2
Functions of secretary IgA
Activation of the complement
through the alternative pathway
Blocking & Neutrilization
opsonization
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-pentameric IgM 5 monomeric connected
by J chain
Pentameric IgM
• 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 1st Ig synthetized by the fetus
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
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
allergen
IgE
FceRI
degranulation
inflammation
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
IgE increases in
• Parasitic infections
• Atopic patients
IL 4 causes switching of Ig to IgE
IL 5 causes eosinophilia
allergen
IgE
FceRI
degranulation
inflammation
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 antiidiotype Ab will be formed (Idiotype
•
antiidiotype network)
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
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
8
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
Clonal Selection of B Cells is Caused by
Antigenic Stimulation
B lymphocyte development (2)
4-Anamnest response :(memory)
The primary I.R. (1st 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
Secondary I.R. (2nd 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
2nd I.R.
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
1st time so no memory cell
*Host exposure for the 2nd
time there is memory cell
*Ab titer decline rapidly
*Ab titer decline slowly
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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