The Rac2 guanosine triphosphatase regulates B lymphocyte antigen receptor responses and chemotaxis and is required for establishment of B-1a and marginal zone B lymphocytes

被引:102
作者
Croker, BA
Tarlinton, DM
Cluse, LA
Tuxen, AJ
Light, A
Yang, FC
Williams, DA
Roberts, AW [1 ]
机构
[1] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, PO Royal Melbourne Hosp, Div Canc & Hematol, Parkville, Vic 3050, Australia
[2] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, PO Royal Melbourne Hosp, Div Immunol, Parkville, Vic 3050, Australia
[3] Univ New S Wales, Sch Microbiol & Immunol, Sydney, NSW, Australia
[4] Indiana Univ, Sch Med,Herman B Wells Ctr Pediat Res, Howard Hughes Med Inst,Dept Pediat, Sect Pediat Hematol Oncol, Indianapolis, IN 46202 USA
[5] Indiana Univ, Sch Med,Herman B Wells Ctr Pediat Res, Howard Hughes Med Inst,Dept Med, Sect Pediat Hematol Oncol, Indianapolis, IN 46202 USA
关键词
D O I
10.4049/jimmunol.168.7.3376
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We have defined roles for the hemopoietic-specific Rho guanosine triphosphatase, Rac2, in B lymphocyte development and function through examination of rac2(-/-) mice. Rac2-deficient mice displayed peripheral blood B lymphocytosis and marked reductions in peritoneal cavity B-la lymphocytes, marginal zone B lymphocytes, and IgM-secreting plasma cells as well as reduced concentrations of serum IgM and IgA. The rac2(-/-) B lymphocytes exhibited reduced calcium flux following coligation of B cell AgR and CD19 and reduced chemotaxis in chemokine gradients. T cell-independent responses to DNP-dextran were of reduced magnitude, but normal kinetics, in rac2(-/-) mice, while T-dependent responses to nitrophenyl-keyhole limpet hemocyanin were subtly abnormal. Rac2 is therefore an essential element in regulating B lymphocyte functions and maintaining B lymphocyte populations in vivo.
引用
收藏
页码:3376 / 3386
页数:11
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