Mechanisms of damage in autoimmunity

Type II Hypersensitivity

• Antibodies are directed against self antigens.
  

• They either
  
1. bind directly to self antigens in tissues (i.e.: myasthenia gravis and Grave’s disease ≫ where receptor is antigen)
   
2. bind to Fc receptors on macrophages and neutrophils inducing inflammation (via complement activation ≫ lysis (i.e.: haemolytic anaemia))
3. opsonise the self antigens ↑ efficiency of phagocytosis.

Type III Hypersensitivity

SLE is a good example here, where anti-nuclear antibodies are formed against cell DNA ≫ immune complexes formed. These are deposited in tissues causing inflammation ≫ tissue destruction. Rheumatoid factor (IgM) deposits in joints and activates complement ≫ cell lysis and also induces inflammation.

Type IV Hypersensitivity

Most autoimmune diseases are Type IV hypersensitivity reactions. It is mediated by T lymphocytes. Basically, antigens interact with naïve T cells which differentiate into Th1 cells. These lie as memory pool cells, and when antigen re-presents Th1 are activated ≫ cytokines produced. Sometimes CD8+ T cells specific for antigen lyse the cell (i.e.: demyelination, Islet destruction, colon cell destruction).

Diagnostic tests

Diagnosis of autoimmune disease is done by testing for autoantibodies. But remember some autoantibodies are harmless, and present no problem. Also autoantibodies are unique to autoimmune diseases. They can be found in TB infections or neoplasia. Also, specific autoantibodies are not unique to specific autoimmune diseases. I.e.: SLE has 80% ANA & 20% RF. RA has >90% RF & 20% ANA.

Category: Pathology Notes