Journal
JOURNAL OF IMMUNOLOGY
Volume 194, Issue 10, Pages 4750-4758Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401634
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Funding
- Swedish Research Council
- Department of Molecular Biosciences, Stockholm University
- Karolinska Institutet
- European Commission 7th Framework Programme
- Ragnar Soderberg Foundation
- Groschinsky Foundation
- Ake Wiberg Foundation
- Bergvall Foundation
- Swedish Society of Medicine
- U.S. Public Health Service Grant [HL-059561]
- Fundacao para a Ciencia e a Tecnologia [SFRH/BD/47926/2008]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/47926/2008] Funding Source: FCT
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The Rho GTPase Cdc42 coordinates regulation of the actin and the microtubule cytoskeleton by binding and activating the Wiskott-Aldrich syndrome protein. We sought to define the role of intrinsic expression of Cdc42 by mature B cells in their activation and function. Mice with inducible deletion of Cdc42 in mature B cells formed smaller germinal centers and had a reduced Ab response, mostly of low affinity to T cell-dependent Ag, compared with wild-type (WT) controls. Spreading formation of long protrusions that contain F-actin, microtubules, and Cdc42-interacting protein 4, and assumption of a dendritic cell morphology in response to anti-CD40 plus IL-4 were impaired in Cdc42-deficient B cells compared with WT B cells. Cdc42-deficient B cells had an intact migratory response to chemokine in vitro, but their homing to the B cell follicles in the spleen in vivo was significantly impaired. Cdc42-deficient B cells induced a skewed cytokine response in CD4(+) T cells, compared with WT B cells. Our results demonstrate a critical role for Cdc42 in the motility of mature B cells, their cognate interaction with T cells, and their differentiation into Ab-producing cells.
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