The process of increasing the ability for phagocytosis of foreign bodies called as:
Opsonins are the substances, which coat the foreign substance and enhance their phagocytosis.
ABOUT COMPLEMENTS I INFLAMMATORY MEDIATORS
· Classical pathway is activated by
IgM (most potent)
IgG (requires 2 molecules)
Activated by immune complexes (eg. in SLE)
· Alternate pathway is antibody independent pathway. It is activated by zymosan, teichoic acid, Agarose, dextrin.
· Third complement pathway: Lectin pathway a/k/a MBL (membrane binding lectin) pathway.
Complement deficiencies & their importance
+ Def of DAF
+ C1 esterase
+ C3 normal C4
+ C3 C4
+ Def of C1 C2 C4
+ Def ofC6 C7 C8
Isolated C9 defect
=> Heriditary angioneurotic edema inhibitor
=> Commonest hereditary complement deficiency
=> Activation of alternate pathway
=> Activation of classical pathway by immune complexes.
=> SLE. Collagen Vasc. disease
=> Neisserial infections
à No Disease
Major serum opsonin
Membrane attack complex (MAC)
SRS-A (slow reacting substances of anaphylaxis)
Leukotriene which is chemotactic
C3b & Fc fragment of IgG
C5-C9 (used in cell lysis)
C5a > C3a, C4a (C5a is more potent)
Lt-C4, D4, E4
LT-B4 (promotes leucocyte adhesion)
LTC4, LTD4, LTE4
PGD2, PGE2, PGI2 PGF2
Hereditary angioneurotic edema: Autosomal dominant; gene involved is SERPING-1 gene on chromosome 11; edema of skin and mucosa.
PNH: pancytopenia and venous thrombosis; lac of glycosyl phosphatidyl inositol which binds to DAF (CD55) & MIRL (CD59); gene is Pig – a gene on X chromosome; mortality due to thrombosis and bone marrow failure.