Abstract
Receptors for the constant fragment (Fc) of IgGs (FcgRs) are largely involved in the pathogenesis of haematological and rheumatic autoimmune disorders, triggering a wide variety of effector functions including phagocytosis, antibody-dependent cellular cytotoxicity, and release of inflammatory mediators, as well as immune complex clearance and regulation of antibody production. The availability of single and multiple Fc-receptor-deficient mice has allowed to get considerable progresses on the in vivo regulation of these responses, through the appreciation of the importance of balancing activation responses with inhibitory signalling. These new insights have a profound impact on our understanding of inflammation in autoimmune diseases, and might lead to new therapeutic approaches for human disorders including Systemic Lupus Erythematosus (SLE) and rheumatoid arthritis.
Keywords: autoimmune diseases, systemic lupus erythematosus
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