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

Jun Zhang; Jian Guo; Ivan Dzhagalov; You Wen He

doi:10.1038/ni1232

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

Jun Zhang, Jian Guo, Ivan Dzhagalov, You Wen He^*

^*Corresponding author for this work

Institute of Microbiology and Immunology

Research output: Contribution to journal › Article › peer-review

47 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	911-919
Number of pages	9
Journal	Nature Immunology
Volume	6
Issue number	9
DOIs	https://doi.org/10.1038/ni1232
State	Published - Sep 2005

Access to Document

10.1038/ni1232

Cite this

@article{0437926d133a40d5bf0908e27df1fc74,

title = "An essential function for the calcium-promoted Ras inactivator in Fcγ receptor-mediated phagocytosis",

abstract = "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.",

author = "Jun Zhang and Jian Guo and Ivan Dzhagalov and He, {You Wen}",

year = "2005",

month = sep,

doi = "10.1038/ni1232",

language = "English",

volume = "6",

pages = "911--919",

journal = "Nature Immunology",

issn = "1529-2908",

number = "9",

}

TY - JOUR

T1 - An essential function for the calcium-promoted Ras inactivator in Fcγ receptor-mediated phagocytosis

AU - Zhang, Jun

AU - Guo, Jian

AU - Dzhagalov, Ivan

AU - He, You Wen

PY - 2005/9

Y1 - 2005/9

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=24944460781&partnerID=8YFLogxK

U2 - 10.1038/ni1232

DO - 10.1038/ni1232

M3 - Article

C2 - 16041389

AN - SCOPUS:24944460781

SN - 1529-2908

VL - 6

SP - 911

EP - 919

JO - Nature Immunology

JF - Nature Immunology

IS - 9

ER -

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

Abstract

Access to Document

Other files and links

Fingerprint

Cite this