Fc-γRI (CD64) contributes substantially to severity of arthritis, hypersensitivity responses, and protection from bacterial infection
Fc-γRI (CD64) contributes substantially to severity of arthritis, hypersensitivity responses, and protection from bacterial infection
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DOI：
10.1016/s1074-7613(02)00294-7
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发表时间：
2002-03-01
期刊：
影响因子：
32.4
通讯作者：
Verbeek, JS
中科院分区：
文献类型：
--
作者：
Ioan-Facsinay, A;de Kimpe, SJ;Verbeek, JS
IgG 高亲和力受体 FcgammaRI 与低亲和力受体 FcgammaRIII 和补体因子具有结合 IgG2a 免疫复合物 (IgG2a-IC) 的能力，这阻碍了其生物学作用的定义。此外，在体内，FcgammaRI 被单体 IgG2a 占据，降低了其对新形成的 IgG2a-IC 的可及性。通过使用多种FcgammaR(-/-)小鼠，我们证明在缺乏FcgammaRI的情况下，IgG2a-IC诱导的细胞吞噬作用、细胞因子释放、细胞毒性和抗原呈递过程受到损害。 FcgammaRI(-/-) 小鼠表现出超敏反应受损、关节炎模型中的软骨破坏大大减少以及对细菌感染的保护受损。我们得出的结论是，FcgammaRI 对多种 IgG2a-IC 依赖性免疫功能和免疫病理反应有显着贡献。
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.