Human Neutrophil Fcγ Receptors Initiate and Play Specialized Nonredundant Roles in Antibody-Mediated Inflammatory Diseases

Naotake Tsuboi, Kenichi Asano, Michael Lauterbach, Tanya N. Mayadas

研究成果: Article査読

122 被引用数 (Scopus)

抄録

Inflammation mediated by antibody-antigen complexes contributes to autoimmune diseases. Mice deficient in the common Fcγ-chain are protected from IgG-mediated glomerulonephritis and the reverse passive Arthus (RPA) reaction and FcR-bearing macrophages, and mast cells have been assigned primary roles in these processes. Here we demonstrate that neutrophil-selective transgenic expression of the two uniquely human neutrophil Fc gamma receptors (FcγRs), FcγRIIA and FcγRIIIB, in Fcγ-chain-deficient mice restored susceptibility to progressive glomerulonephritis and the cutaneous RPA reaction. FcγRIIIB and FcγRIIA mediated neutrophil accumulation, whereas FcγRIIA alone promoted organ injury. In a model of soluble immune complexes deposited within the vasculature, FcγRIIIB was responsible for neutrophil slow rolling and adhesion whereas in the cremaster RPA, induced by both vascular and tissue soluble immune complexes, FcγRIIA predominated. Thus, human FcγRs on neutrophils serve as molecular links between antibody and immunological disease, with FcγRIIA promoting tissue injury and FcγRIIIB and FcγRIIA displaying specialized context-dependent functions in neutrophil recruitment.

本文言語English
ページ(範囲)833-846
ページ数14
ジャーナルImmunity
28
6
DOI
出版ステータスPublished - 13-06-2008
外部発表はい

All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学
  • 感染症

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