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
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
收藏
页码:911 / 919
页数:9
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