| Literature DB >> 25870239 |
Natalija Gerasimcik1, Carin I M Dahlberg2, Marisa A P Baptista2, Michel J Massaad3, Raif S Geha3, Lisa S Westerberg2, Eva Severinson4.
Abstract
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.Entities:
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Year: 2015 PMID: 25870239 PMCID: PMC4416737 DOI: 10.4049/jimmunol.1401634
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422