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 FcγR-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 FcγR-mediated phagocytosis. CAPRI-deficient mice had an impaired innate immune response to bacterial infection. These results suggest that CAPRI provides a link between FcγR and Cdc42 and Rac1 and is essential for innate immune responses.
原文 | English |
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頁(從 - 到) | 911-919 |
頁數 | 9 |
期刊 | Nature Immunology |
卷 | 6 |
發行號 | 9 |
DOIs | |
出版狀態 | Published - 9月 2005 |