Nature Immunology
6, 911 - 919 (2005)
Published online: 24 July 2005; | doi:10.1038/ni1232
An essential function for the calcium-promoted Ras inactivator in Fc receptor−mediated phagocytosisJun Zhang1, 2, Jian Guo1, 2, Ivan Dzhagalov1
& You-Wen He11
Department of Immunology, Duke University Medical Center, Durham, North Carolina
27710, USA. 2
These authors contributed equally to this work.
Correspondence should be addressed to You-Wen He he000004@mc.duke.edu 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 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 FcR-mediated phagocytosis. CAPRI-deficient mice had an impaired innate immune response to bacterial infection. These results suggest that CAPRI provides a link between FcR and Cdc42 and Rac1 and is essential for innate immune responses.
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