Type III hypersensitivity reaction is caused by thegeneration 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, theoverproduction of immune complexes makes the complexes hard to be removed thuslead to type III hypersensitivity reactions. The inefficient clearance ofimmune complexes will lead to the deposition of the complexes on the tissue orblood vessel (Owen, Punt, Stranford & Jones, 2013).It has also been stated that, type III hypersensitivityis further characterized by the deposition of immune complex on a non-specifictissue and the reaction occurs when the immune and phagocytic system are unableto effectively removed the immune complex (Copstead& Banasik, 2014). The deposition of the immunecomplex on the tissue will make it difficult for the phagocytic cell to removeit thus; the immune complex will subsequently activate the classicallyactivated complement system which releases numerous inflammatory mediators thatrecruit, activate and degranulate neutrophils Eggleton,2013) .In fact, the activation of complement byantigen-antibody complex as well as the release of lytic enzyme by neutrophilsis the main cause for the tissue damage for the type III hypersensitivityreaction (Lydyard, Whelan & Fanger, 2011).            The activation ofclassically activated complement system by antigen-antibody complex starts withthe activation of C1. The activated C1 then convert the inactive C4 and C2 toC3 convertase (C4b2b).

The C3 convertase then convert the C3 to C3a and C3b(Todd & Spickett, 2010). The C3b (opsonin) will attracts the neutrophilswhich released the lysosomal enzyme (MD, n.d.).

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The C3b will bind with C3 convertase to form C5 convertase (C4b2b3b). The C5convertase will convert C5 to C5a and C5b (Todd & Spickett, 2010). The C3aand C5a is a chemotactic factor which involve in the recruitment of theneutrophils to the site of reaction (Rao, 2002).

The C5b will then bind with C6, C7, C8 and C9 forming the membraneattack complex C5 to C9 (Todd & Spickett, 2010). The activation of membraneattack complex destructs the tissue where the immune complex deposited (Rao, 2002). This clearly explains the role ofactivation of complement in type III hypersensitivity reaction.

Next, the neutrophils that have been recruited at thesite of immune complex deposition will release lysosomal enzyme due tounsuccessful attempt of phagocytosis of the immune complex attached on thebasement membrane. The lytic enzyme that has been released out of neutrophilswill digest the immune complex and lead to the destruction of the tissue at thevicinity as well (Rao, 2002).To sum up, the activation of complement system is the mechanism of the type IIIhypersensitivity reaction and it involves several complements and inflammatorycell to remove the antigen-antibody complex.


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