An essential function for the calcium-promoted Ras inactivator in Fcγ receptor-mediated phagocytosis

被引：46

作者：

Zhang, J ^{[1
]}

Guo, J ^{[1
]}

Dzhagalov, I ^{[1
]}

He, YW ^{[1
]}

机构：

[1] Duke Univ, Med Ctr, Dept Immunol, Durham, NC 27710 USA

来源：

NATURE IMMUNOLOGY | 2005年 / 6卷 / 09期

关键词：

D O I：

10.1038/ni1232

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Fc receptor ( FcR) - mediated phagocytosis requires activation of the Rho GTPases Cdc42 and Rac1, but how they are recruited to the FcR is unknown. Here we show that the calcium- promoted Ras inactivator ( CAPRI), a Ras GTPase- activating protein, functions as an adaptor for Cdc42 and Rac1 during FcR- mediated phagocytosis. CAPRI- deficient macrophages had impaired Fc gamma R- mediated phagocytosis and oxidative burst, as well as defective activation of Cdc42 and Rac1. CAPRI interacted constitutively with both Cdc42 and Rac1 and translocated to phagocytic cups during Fc gamma R- mediated phagocytosis. CAPRI-deficient mice had an impaired innate immune response to bacterial infection. These results suggest that CAPRI provides a link between Fc gamma R and Cdc42 and Rac1 and is essential for innate immune responses.

引用

页码：911 / 919

页数：9

共 32 条

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