First of all, the reaction between antibodies (IgG orIgM) and soluble antigens in the serum resulted in the formation of circulatingantigens-antibody complex (Abbas & Lichtman, 2011). The soluble immunecomplex are usually cleared and removed by the phagocytic cells. However, insome cases, due to large amount of immune complex formed, the immune complexcannot be easily removed by the phagocytic cell and may be deposited in vesselwalls or extravascular tissues (Rao, 2002). The deposition of immune complexcan lead to tissue damage mainly due to the antibody-mediated complementactivation and release of lytic enzymes from neutrophils (Lydyard, Whelan &Fanger, 2011). This immune complex-mediated tissue damage is called as Type IIIhypersensitivity or also known as Immune complex hypersensitivity.

            The antigen-antibody complexactivates the complement system via the classical pathway which will release thecomplement byproducts that recruit leukocytes and induce inflammation. First,the immune complex will activate the C1 which later will activate the C4 and C2to produce C4b2b (C3 convertase).The C3 convertase then will convert C3 to C3aand C3b. The C3b with C4b2b will form C4b2b3b (C5 convertase) which will thenconvert C5 into C5a and C5b.

The C5b with C6, C7, C8 and C9 will form C5-9which also known as membrane attack complex (Todd & Spickett, 2010).            The C3a and C5a acts as thechemotactic factors that attract the neutrophils to the site of immune complexdeposition (Rao, 2002). Meanwhile, C3b act as opsonin that enhancesphagocytosis (Todd & Spickett, 2010). If the immune complexes bind to cellsuch as red blood cells and platelets, the C3b will opsonised the cells. Then,the cells may be ingested and destroyed by the phagocytes (neutrophils) as thereactive oxygen species (ROS) and lysosomal enzyme released in thephagolysosome (Abbas & Lichtman, 2011). However, if the immune complexesattached to the basement membrane, the phagocytosis process will be interfered.This causes the neutrophils to release lytic enzyme in the extracellular spacesdue to fail attempt of phagocytosis.

The release of the lytic enzyme along withthe membrane attack complex of the complement will then damage the tissueswhere the immune complex are deposited and also the adjacent tissues (Rao,2002). Hence, it can be concluded that the Type III hypersensitivity related tothe tissue damage due to immune complex-mediated reaction.

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