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FcgammaRI (CD64) contributes substantially to severity of arthritis, hypersensitivity responses, and protection from bacterial infection

Ioan-Facsinay, A.
de Kimpe, S. J.
Hellwig, S. M.
van Lent, P. L.
Hofhuis, F. M.
van Ojik, H. H.
Sedlik, C.
da Silveira, S. A.
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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 AnimalsArthritis, Experimental/genetics/ immunology/pathologyBordetella pertussis/ immunologyCartilage/pathologyFemaleHypersensitivity/genetics/ immunologyImmunity/geneticsImmunoglobulin G/immunologyMiceMice, Inbred C57BLMice, KnockoutReceptors, IgG/genetics/ immunologyWhooping Cough/ immunology
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PMID: 11911824
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