HIGH YIELD POINT FOR BASIC IMMUNOLOGY 2015

HIGH YIELD POINT FOR BASIC IMMUNOLOGY  2015

HIGH YIELD POINT FOR BASIC IMMUNOLOGY  2015

 

Human leukocyte antigens and different classes:

The human leukocyte antigen system (HLA) is the name of the major histocompatibility complex

(MHC) in humans. It is located on chromosome 6. Two different classes.

HLA class 1 [MHC-1]: HLA-A, HLA-B, HLA-C

HLA class 2 [MHC-2]: HLA-DP, HLA-DQ, HLA-DR

Location of MHC-1 & MHC-2 antigens:

MHC-1: All nucleated cells & platelets (NO MHC on RBC)

MHC-2: Antigen Presenting cells (Dendritic cells, langerhans cells, activated macrophage, B-cells, activated T-cells & activated endothelial cells)

Important-

MHC-1 is necessary for antigen recognition by CD8+ T-cells

MHC-2 is necessary for antigen recognition by CD4+ T-cells

Difference:

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)

 

Complement system:

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.