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FcγRIII(CD16)缺陷小鼠中IgG依赖性过敏反应和阿瑟斯反应受损。

Impaired IgG-dependent anaphylaxis and Arthus reaction in Fc gamma RIII (CD16) deficient mice.

作者信息

Hazenbos W L, Gessner J E, Hofhuis F M, Kuipers H, Meyer D, Heijnen I A, Schmidt R E, Sandor M, Capel P J, Daëron M, van de Winkel J G, Verbeek J S

机构信息

Department of Immunology, University Hospital Utrecht, The Netherlands.

出版信息

Immunity. 1996 Aug;5(2):181-8. doi: 10.1016/s1074-7613(00)80494-x.

Abstract

The family of receptors for IgG (Fc gamma R) plays an essential role in antibody-mediated effector functions of the immune system. However, the specific contribution of each of the Fc gamma R classes to in vivo immune reactions is still unclear. Here, we demonstrate that mice deficient for the ligand-binding alpha chain of Fc gamma RIII lack NK cell-mediated antibody-dependent cytotoxicity and phagocytosis of IgG1-coated particles by macrophages. Strikingly, these mice lack IgG-mediated mast cell degranulation, are resistant to IgG-dependent passive cutaneous anaphylaxis, and exhibit an impaired Arthus reaction. These results indicate a prominent role for Fc gamma RIII in inflammatory and anaphylactic responses, making this receptor a potential target in immunotherapy.

摘要

免疫球蛋白G(IgG)受体家族(FcγR)在免疫系统的抗体介导效应功能中起关键作用。然而,FcγR各亚类对体内免疫反应的具体贡献仍不清楚。在此,我们证明FcγRIII配体结合α链缺陷的小鼠缺乏自然杀伤(NK)细胞介导的抗体依赖性细胞毒性以及巨噬细胞对IgG1包被颗粒的吞噬作用。引人注目的是这些小鼠缺乏IgG介导的肥大细胞脱颗粒,对IgG依赖性被动皮肤过敏反应具有抗性,并且表现出阿图斯反应受损。这些结果表明FcγRIII在炎症和过敏反应中起重要作用,使该受体成为免疫治疗的潜在靶点。

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