MHC-1 is necessary for antigen recognition by CD8+ T-cells
MHC-2 is necessary for antigen recognition by CD4+ T-cells
MHC-1: React with ENDOGENOUSLY produce peptides by virus, intracellular bacteria, intracellular parasites and tumor cells
MHC-2: React with EXOGENOUSLY PROCESSED antigens
Handling of organisms:
MHC-1: It works with intracellular organisms so after reacting with endogenously processed antigen, β2
microglobulin transports MHC class-1 molecules to the cell surface where it can be recognized by CD 8
T-cells and organisms are then killed by CD8 T-cells
MHC-2: It works with Extracellular organisms so once organisms engulfed, MHC class-2 molecule fuse with vacuole containing exogenously processed antigen, invariant chain is released and MHC-2-peptide complex is then transported to the cell surface where it can be recognized by CD 4 T-cells. Invariant chain prevents interaction b/w endogenously produced peptide and MHC-2 molecules intracellularly
How does ADCC [Antibody Dependent Cellular Cytotoxicity] and NK cells mediated cytotoxicity differed?
ADCC: IgG + NK cells → use CD 16 molecule (Fc receptor) to identify target cells.
NK cells mediated cytotoxicity: use CD 56 (No antibody involve Ex.- lysis of infected RBC)
Classical Pathway: activated by antigen-Ab reaction (IgG & IgM, IgM most efficient) [start point C1] [C1 – C4 – C2 – C3] [C4bC2a is C3-convertase] [C4bC2aC3b (C5-convertase) splits C5 into C5a & C5b which then form C5b,6,7,8,9]
Alternative Pathway: C3 hydrolyze spontaneously in our body into C3a & C3b. If there is a pathogenic membrane surface nearby, C3b binds to it. If not, both C3a & C3b rejoin. Upon binding with a cellular membrane, C3b is bound by factor B to form C3bB. This complex in presence of factor D will be cleaved into Ba and Bb. Bb will remain covalently bonded to C3b to form C3bBb which is the alternative pathway C3-convertase.