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FcgammaRI (CD64) contributes substantially to severity of arthritis, hypersensitivity responses, and protection from bacterial infection
|Published in||Immunity. 2002, vol. 16, no. 3, p. 391-402|
|Abstract||The high-affinity receptor for IgG, FcgammaRI, shares its capacity to bind IgG2a immune complexes (IgG2a-IC) with the low-affinity receptor FcgammaRIII and complement factors, hampering the definition of its biological role. Moreover, in vivo, FcgammaRI is occupied by monomeric IgG2a, reducing its accessibility to newly formed IgG2a-IC. By using a variety of FcgammaR(-/-) mice, we demonstrate that in the absence of FcgammaRI, the IgG2a-IC-induced cellular processes of phagocytosis, cytokine release, cellular cytotoxicity, and antigen presentation are impaired. FcgammaRI(-/-) mice showed impaired hypersensitivity responses, strongly reduced cartilage destruction in an arthritis model, and impaired protection from a bacterial infection. We conclude that FcgammaRI contributes substantially to a variety of IgG2a-IC-dependent immune functions and immunopathological responses.|
|Keywords||Animals — Arthritis, Experimental/genetics/ immunology/pathology — Bordetella pertussis/ immunology — Cartilage/pathology — Female — Hypersensitivity/genetics/ immunology — Immunity/genetics — Immunoglobulin G/immunology — Mice — Mice, Inbred C57BL — Mice, Knockout — Receptors, IgG/genetics/ immunology — Whooping Cough/ immunology|