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CD5介导的B-1 B细胞中抗原受体诱导的生长信号的负调控。

CD5-mediated negative regulation of antigen receptor-induced growth signals in B-1 B cells.

作者信息

Bikah G, Carey J, Ciallella J R, Tarakhovsky A, Bondada S

机构信息

Department of Microbiology and Immunology and Center on Aging, University of Kentucky, Lexington, KY 40536, USA.

出版信息

Science. 1996 Dec 13;274(5294):1906-9. doi: 10.1126/science.274.5294.1906.

Abstract

A subset of B lymphocytes present primarily in the peritoneal and pleural cavities is defined by the expression of CD5 and is elevated in autoimmune diseases. Upon signaling through membrane immunoglobulin M (mIgM), splenic B lymphocytes (B-2) proliferate, whereas peritoneal B cells (B-1) undergo apoptosis. However, in CD5-deficient mice, B-1 cells responded to mIgM crosslinking by developing a resistance to apoptosis and entering the cell cycle. In wild-type B-1 cells, prevention of association between CD5 and mIgM rescued their growth response to mIgM crosslinking. Thus the B cell receptor-mediated signaling is negatively regulated by CD5 in normal B-1 cells.

摘要

主要存在于腹腔和胸腔的一部分B淋巴细胞由CD5的表达所定义,且在自身免疫性疾病中数量增加。通过膜免疫球蛋白M(mIgM)发出信号后,脾脏B淋巴细胞(B-2)会增殖,而腹膜B细胞(B-1)则会发生凋亡。然而,在缺乏CD5的小鼠中,B-1细胞通过产生抗凋亡能力并进入细胞周期来对mIgM交联作出反应。在野生型B-1细胞中,阻止CD5与mIgM之间的结合可挽救它们对mIgM交联的生长反应。因此,在正常B-1细胞中,B细胞受体介导的信号传导受到CD5的负调控。

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