Type the immune and phagocytic system are unable

Type III hypersensitivity reaction is caused by the
generation of antigen-antibody immune complex from the interaction of antigen
(foreign serum product, self-antigen or microbial antigen) with the antibody
(IgG or IgM) that may lead to phagocytic or complement-mediated destruction (Lydyard, Whelan & Fanger, 2011).
Generally, the immune complex will be removed by phagocytic cells, however, the
overproduction of immune complexes makes the complexes hard to be removed thus
lead to type III hypersensitivity reactions. The inefficient clearance of
immune complexes will lead to the deposition of the complexes on the tissue or
blood vessel (Owen, Punt, Stranford & Jones, 2013).

It has also been stated that, type III hypersensitivity
is further characterized by the deposition of immune complex on a non-specific
tissue and the reaction occurs when the immune and phagocytic system are unable
to effectively removed the immune complex (Copstead
& Banasik, 2014). The deposition of the immune
complex on the tissue will make it difficult for the phagocytic cell to remove
it thus; the immune complex will subsequently activate the classically
activated complement system which releases numerous inflammatory mediators that
recruit, activate and degranulate neutrophils Eggleton,
2013) .In fact, the activation of complement by
antigen-antibody complex as well as the release of lytic enzyme by neutrophils
is the main cause for the tissue damage for the type III hypersensitivity
reaction (Lydyard, Whelan & Fanger, 2011).

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            The activation of
classically activated complement system by antigen-antibody complex starts with
the activation of C1. The activated C1 then convert the inactive C4 and C2 to
C3 convertase (C4b2b). The C3 convertase then convert the C3 to C3a and C3b
(Todd & Spickett, 2010). The C3b (opsonin) will attracts the neutrophils
which released the lysosomal enzyme (MD, n.d.).
The C3b will bind with C3 convertase to form C5 convertase (C4b2b3b). The C5
convertase will convert C5 to C5a and C5b (Todd & Spickett, 2010). The C3a
and C5a is a chemotactic factor which involve in the recruitment of the
neutrophils to the site of reaction (Rao, 2002). The C5b will then bind with C6, C7, C8 and C9 forming the membrane
attack complex C5 to C9 (Todd & Spickett, 2010). The activation of membrane
attack complex destructs the tissue where the immune complex deposited (Rao, 2002). This clearly explains the role of
activation of complement in type III hypersensitivity reaction.

Next, the neutrophils that have been recruited at the
site of immune complex deposition will release lysosomal enzyme due to
unsuccessful attempt of phagocytosis of the immune complex attached on the
basement membrane. The lytic enzyme that has been released out of neutrophils
will digest the immune complex and lead to the destruction of the tissue at the
vicinity as well (Rao, 2002).
To sum up, the activation of complement system is the mechanism of the type III
hypersensitivity reaction and it involves several complements and inflammatory
cell to remove the antigen-antibody complex.