Infections are strongly
associated with autoimmune disease and seem to initiate them either by the
process of molecular mimicry or the bystander effect [1].
Molecular mimicry is where the
immune system develops antibodies to a particular amino acid sequence expressed
by a pathogen, which happens to be structurally similar enough for the
antibodies to cross react with self-antigens, our own tissues.
The bystander effect is where
an infection leads to inflammation and tissue damage. Then this infected and damaged tissue is
considered foreign by the immune system, antibodies are made against it, but
these antibodies are cross-reactive with nearby undamaged tissue.
Molecular mimicry and the
bystander effect are observed in animal models of autoimmune disease [1]. But these mechanisms are incomplete for two
reasons.
1.
Why does the immune system continue to attack the body after the pathogen has been destroyed?
2.
Why has the incidence of autoimmune disease
increased while infectious disease has decreased?