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Receptors for the Fc domains of IgG (Fc gamma R) play a critical role in linking humoral and cellular immune responses. The various Fc gamma R genes may contribute to differences in infectious and immune related diseases in various ethnic populations. Polymorphisms of Fc gamma R mainly Fc gamma R IIA, IIB, IIIA, IIIB have been identified as genetic factors influencing susceptibility to disease or disease course of a prototype autoimmune disease like Systemic Lupus Erythematosus (SLE). Activated and inhibitory Fc gamma Rs seem to play an important role in the pathogenesis of SLE, in initiation of autoimmunity, the subsequent development of inflammatory lesions and finally immune clearance mechanisms. This review focuses on the role of Fc gamma R polymorphism and their association with clinical manifestations and initiation of autoantibody production, inflammatory handling of immune complexes and disease development in SLE patients.

Fc gamma receptor polymorphisms in systemic lupus erythematosus and their correlation with the clinical severity of the disease