Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10265
Title: FcgammaRII and multi-system autoimmune disease.
Authors: van de Velde, Nicholas C;Mottram, Patricia L;Hogarth, P Mark
Affiliation: Burnet Institute (Austin Campus), Austin Hospital, Studley Road, Heidelberg, Victoria, 3084, Australia, pm.hogarth@burnet.edu.au.
Issue Date: 8-Nov-2006
Citation: Springer Seminars in Immunopathology 2006; 28(4): 329-38
Abstract: The FcR are a crucial link in the immune response between humoral and cellular immunity and cell-based effector systems, mediating a wide variety of physiological and biochemical responses. The FcR for IgG (FcgammaR) and in particular the most widely expressed of these, FcgammaRII, are important in regulating adaptive immunity. Disruption of their function is a key factor in the development of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), which are characterized by chronic, multi-organ inflammation. Studies of the FcgammaRII include structure/function relationships, investigation of the associations between FcR polymorphisms and human disease and animal studies using knockout or transgenic mouse models. These investigations showed that the various forms of FcgammaRII interact with immune complexes to either initiate or inhibit inflammation. In conjunction with environmental antigens and genotype, the FcgammaRII activating and inhibitory receptors determine the nature and magnitude of response to antigens. In this review, the structure and function of the FcgammaRIIs and their role in immune complex-mediated auto-immunity are discussed.
Internal ID Number: 17091247
URI: http://ahro.austin.org.au/austinjspui/handle/1/10265
DOI: 10.1007/s00281-006-0056-x
URL: http://www.ncbi.nlm.nih.gov/pubmed/17091247
Type: Journal Article
Appears in Collections:Journal articles

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