Fc-γRI-deficient mice show multiple alterations to inflammatory and immune responses
Fc-γRI-deficient mice show multiple alterations to inflammatory and immune responses
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DOI：
10.1016/s1074-7613(02)00287-x
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发表时间：
2002-03-01
期刊：
影响因子：
32.4
通讯作者：
Hogarth, PM
中科院分区：
文献类型：
--
作者：
Barnes, N;Gavin, AL;Hogarth, PM
小鼠高亲和力IgG Fc受体FcgammaRI的失活导致抗体Fc依赖性功能的广泛缺陷。这些研究表明，Fc γ RI在单体IgG的内吞作用、动力学和免疫复合物的吞噬程度、基于巨噬细胞的ADCC和免疫复合物依赖性抗原呈递给致敏T细胞中具有首要重要性。在不存在Fc γ RI的情况下，抗体应答升高，这意味着通过缺失Fc γ RI去除了控制点。此外，发现FcR-γ链缺陷小鼠表达部分功能性FcgammaRI。因此，Fc γ RI是Fc依赖性细胞活化和免疫应答发展的早期参与者。
The inactivation of the mouse high-affinity IgG Fc receptor FcgammaRI resulted in a wide range of defects in antibody Fc-dependent functions. These studies showed the primary importance of FcgammaRI in endocytosis of monomeric IgG, kinetics, and extent of phagocytosis of immune complexes, in macrophage-based ADCC, and in immune complex-dependent antigen presentation to primed T cells. In the absence of FcgammaRI, antibody responses were elevated, implying the removal of a control point by the deletion of FcgammaRI. In addition, FcR-gamma chain-deficient mice were found to express partially functional FcgammaRI. Thus, FcgammaRI is an early participant in Fc-dependent cell activation and in the development of immune responses.