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Adaptive Immunity: Mateen Irfansha
Adaptive Immunity: Mateen Irfansha
Adaptive Immunity: Mateen Irfansha
MATEEN IRFANSHA
Adaptive immunity :-
Adaptive immunity is induced as a response against a specific
antigen, after the collaboration among phagocytic cells,T and B
lymphocytes and the production of immunoglobulins and
lymphokines (IL).
Q. Differences bitween Innate immunity & Adaptive immunity?
1. Humoral immunity .
2. Cell-mediated immunity.
Humoral immunity :- (Humoral immunity block extrtracellular microbes)
immunity that is mediated by secreted antibodies produced in the B cells . B Cells
(with co-stimulation) transform into plasma cells which secrete antibodies. Humoral
immunity is so named because it involves substances found in the humours, or
body fluids.
Exogenous antigens
Cell-mediated immunity :-
Cell mediated immunity is an immune response that does not
involve antibodies but rather involves the activation of phagocytes ,
natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and
the release of various cytokines in response to an antigen.
Endogenous antigens
Abbas, Lichtman and Pillai. Cellular and Molecular Immunology, 7th edition, 2011
(1) Destroy all cells (even host cells) in the activation area,
Bacterial
Antibodies surface
6 molecules of C1q
2 molecules of C1r
2 molecules of C1s
Antigens
C4bC2b/C3 convertase
C4bC2b
C2 is cleaved into
oC2b, which binds noncovalently to a site
on C4b, leaving an inactive fragment of
oC2a
The complex of C4b.2b is called "C3 convertase"
because it catalyzes the cleavage of C3.
C4bC2bC3b/C5
C3a Convertase
C3b
C3b
C5a
C5b
C9
C7
C8
By direct opsonisation.
By indirect opsonisation.
Q.HOW ANTIBODY KILLS BACTERIAS?
By direct opsonisation :-
FC receptors
Antibody Macrophages/
neutrophilis
Gram +ve bacteria
By indirect opsonisation:-
C3b receptors
Antibody Macrophages/
neutrophilis
Gram +ve bacteria
By activating complement system till MAC formation:-
C3a
C5a
C3 convertase
Antibody
C5 convertase
MAC
Gram ve bacteria
Q. What is ABO incompatible blood transfusion?
C3 Convertase C5 Convertase
Clinical significans:-
Aggregation of IgA can cause activation of alternate pathway.
Diseases related with IgA aggregations are..
2.Dermititus Herpetiformus.
3.Henoshawlin Purpura.
Mannan-binding lectin pathway
issimilar in structure to the classical complement pathway in
that, after activation, it proceeds through the action of C4 and C2
to produce activated complement proteins further down the
cascade.
it is not antibody-dependent.
MASP-1(similar to C1r)
MASP-2 (similar to C1s)
C3 convertase :-
C4b and C2b combine on the surface of the pathogen to
form C3 convertase (C4bC2b).
while C4a and C2a act as chemoattractants.
C5 convertase:-. C4bC2bC3b, which is a C5 convertase
and can start the assembly of the membrane attack
complex
Clinical significance :-
has been found that people deficient in MBL experience a
substantial increase in infections during the early years of
childhood .
Regulation of Complement Activity:-
The explosive potential of the complement system requires that
it be kept under tight control.
At least 12 proteins are known that do this.
Three examples:
Factor H removes Bb from the alternative pathway .
With so many proteins involved, it is not surprising that inherited deficiencies of one
or another are sometimes encountered in humans.
examples:
C2 & C4. Curiously, immune complex disorders, with a deficiency of C2 (or of one of
the other "early" components like C1q, C1r, C1s, or C4). This is frequently found in
patients with the immune complex disorders (autoimmune disorder) system lupus
erythematosus (SLE).
Defficency of C5b,C6,C7,C8,C9 & lectin pathway lead to Gram ve
infections (Nesierrial infection)
C1INH. A deficiency of C1INH produces hereditary
angioneurotic edema (HANE). Patients are at risk of
occasional explosive triggering of the complement system.