Gerasimcik Natalija, Dahlberg Carin I M, Baptista Marisa A P, Massaad Michel J, Geha Raif S, Westerberg Lisa S, Severinson Eva
Department of Molecular Biosciences, Wenner-Gren Institute, Stockholm University, SE-106 91 Stockholm, Sweden;
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, SE-171 77 Stockholm, Sweden;
J Immunol. 2015 May 15;194(10):4750-8. doi: 10.4049/jimmunol.1401634. Epub 2015 Apr 13.
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.
Rho GTP酶Cdc42通过结合并激活威斯科特-奥尔德里奇综合征蛋白来协调肌动蛋白和微管细胞骨架的调节。我们试图确定成熟B细胞中Cdc42的内在表达在其激活和功能中的作用。与野生型(WT)对照相比,成熟B细胞中可诱导缺失Cdc42的小鼠形成的生发中心较小,抗体反应降低,且大多对T细胞依赖性抗原的亲和力较低。与WT B细胞相比,Cdc42缺陷型B细胞在响应抗CD40加IL-4时,包含F-肌动蛋白、微管和Cdc42相互作用蛋白4的长突起的铺展形成以及树突状细胞形态的呈现均受损。Cdc42缺陷型B细胞在体外对趋化因子具有完整的迁移反应,但其在体内归巢至脾脏中的B细胞滤泡的能力显著受损。与WT B细胞相比,Cdc42缺陷型B细胞在CD4(+) T细胞中诱导了偏向性的细胞因子反应。我们的结果证明Cdc42在成熟B细胞的运动性、它们与T细胞的同源相互作用以及它们分化为产生抗体的细胞中起关键作用。