Turning now to Type III hypersensitivity
- immune complex mediated.
This can result in the activation of macrophages, the
recruitment and activation of neutrophils, immune complexes
can get trapped in very small locations like the glomeruli
of kidney, small blood vessels in the skin and so forth.
And cause pathological damage.
So some examples of type III hypersensitivity
- systemic lupus erythematosus
(SLE) which is characterized by the
development of anti-nuclear antibodies.
These are antibodies against a range of different antigens
present in the nucleus such as DNA, histones and so on.
Post-streptococcal glomerulonephritis which is due
to a reaction to streptococcal cell wall antigens.
Serum sickness caused by exposure to foreign
antiserum, for example a horse anti-snake venom.
And polyarteritis nodosa which can occur in response to hepatitis
B virus surface antigen stimulation of a immune response.
Immune complex mediated tissue injury happens when the
circulating immune complexes get deposited in blood vessels.
Complement and Fc receptor-mediated recruitment
and activation of inflammatory cells occurs.
There are lysosomal
enzymes that are released.
Reactive oxygen species being produced by
neutrophils, and the end result is a vasculitis.
And here we have some examples of the trouble that
immune complexes can cause in type III hypersensitivity.
Activation of complement leading to the activation
of macrophages and neutrophils with the release
of inflammatory mediators, of reactive oxygen
intermediates, proteolytic enzymes and so forth.
A whole load of potentially damaging substances
released from these macrophages and neutrophils.
Following complement activation due
to the formation of immune complexes,
anaphylatoxins, complement component C3a and
C5a can cause the activation of mast cells.
Also, platelets can become
activated and aggregate.