Immune escape mechanisms

Bacteria

Bacteria can vary their antigenic material known as antigenic variation – i.e.: E.coli. Avoidance of complement mediated damage:

1) outer capsule of microbe not penetrable

2) outer surface configuration does not allow C3b binding,

3) diversionary structures (decoy cytokine receptors, or antibody binding to diversionary structure doesn’t do anything),

4) produce enzymes that degrade complement products,

5) resistance to MAC forming + inserting,

6) secreting decoy proteins so complement binding is diverted from binding to bacteria.

Resistance to phagocytosis:

1. phagocytosis requires chemotaxis, but toxins repel/prevent chemotaxis therefore phagocytes don’t come near infection,
   
2. bacteria may have outer coats that inhibits phagocytosis (i.e.: Pneumococcus),
   
3. inhibit phagolysosome fusion and escape from vesicles of phagocytes into cytosol.

Viruses

Antigenic drift (influenza), blocking complement system (i.e.: HSV produces C3b binding protein and augments decay of C3bBb), immunosuppressive cytokines (Epstein Barr virus), cytokine receptor homologue (Vaccinia, CMV), inhibits antigen processing pathway (i.e.: CMV), infects immune cells.

Parasites

Sequestered in a particular anatomical position so difficult access, avoids phagocytosis, antigenic variation – avoids recognition, it somehow has same surface antigens of host so immune system thinks its also part of host, suppresses immune system, lymphocytoxic factor, release spores that can mop up any antibody.

Category: Pathology Notes