Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies.
Contribution of Human FcγRs to Disease with Evidence from Human Polymorphisms and Transgenic Animal Studies.
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DOI：
10.3389/fimmu.2014.00254
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发表时间：
2014
影响因子：
7.3
通讯作者：
Bruhns P
中科院分区：
文献类型：
--
作者：
Gillis C;Gouel-Chéron A;Jönsson F;Bruhns P
人IgG抗体的生物活性主要依赖于IgG Fc部分的受体家族，即Fcγ R：FcγRI、Fcγ RIIA、Fc γ RIIB、Fc γ RIIC、Fc γ RIIIA、FcγRIIIB、FcRL 5、FcRn和TRIM 21。所有Fcγ R均在细胞表面结合IgG，但FcRn和TRIM 21除外，其在内化后结合IgG。Fcγ R对IgG的亲和力由人Fcγ R的多态性决定，范围为2 × 104至8 × 107 M−1。Fcγ R的生物学功能从细胞活化或抑制、IgG内化/内吞/吞噬到IgG转运和再循环。本综述主要关注人Fcγ R，并对目前对这些受体如何参与各种病理学的理解进行概述。它将定义Fcγ R及其多态性变体，它们对人IgG亚类的亲和力，并审查FcγR多态性与人类病理学之间的关联。还将描述已用于研究这些受体在自身免疫性、炎症性和过敏性疾病模型中的作用的人Fcγ R转基因小鼠。
The biological activities of human IgG antibodies predominantly rely on a family of receptors for the Fc portion of IgG, FcγRs: FcγRI, FcγRIIA, FcγRIIB, FcγRIIC, FcγRIIIA, FcγRIIIB, FcRL5, FcRn, and TRIM21. All FcγRs bind IgG at the cell surface, except FcRn and TRIM21 that bind IgG once internalized. The affinity of FcγRs for IgG is determined by polymorphisms of human FcγRs and ranges from 2 × 104 to 8 × 107 M−1. The biological functions of FcγRs extend from cellular activation or inhibition, IgG-internalization/endocytosis/phagocytosis to IgG transport and recycling. This review focuses on human FcγRs and intends to present an overview of the current understanding of how these receptors may contribute to various pathologies. It will define FcγRs and their polymorphic variants, their affinity for human IgG subclasses, and review the associations found between FcγR polymorphisms and human pathologies. It will also describe the human FcγR-transgenic mice that have been used to study the role of these receptors in autoimmune, inflammatory, and allergic disease models.