CD72-deficient mice reveal nonredundant roles of CD72 in B cell development and activation

被引：166

作者：

Pan, C

Baumgarth, N

Parnes, JR ^{[1
]}

机构：

[1] Stanford Univ, Sch Med, Dept Med, Div Rheumatol & Immunol, Stanford, CA 94305 USA

[2] Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA

来源：

IMMUNITY | 1999年 / 11卷 / 04期

关键词：

D O I：

10.1016/S1074-7613(00)80124-7

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

CD72, a B cell surface protein of the C-type lectin superfamily, recruits the tyrosine phosphatase SHP-1 through its ITIM motif(s). Using CD72-deficient (CD72(-/-)) mice, we demonstrate that CD72 is a nonredundant regulator of B cell development. In the bone marrow of CD72(-/-) mice, there was a reduction in the number of mature recirculating B cells and an accumulation of pre-B cells. In the periphery of CD72(-/-) mice, there were fewer mature B-2 cells and more B-l cells. In addition, CD72 is a negative regulator of B cell activation, as CD72(-/-) B cells were hyperproliferative in response to various stimuli and showed enhanced kinetics in their intracellular Ca2+ response following IgM cross-linking.

引用

页码：495 / 506

页数：12

共 58 条

[1]

Adachi T, 1998, J IMMUNOL, V160, P4662

[2] Disruption of the Cr2 locus results in a reduction in B-1a cells and in an impaired B cell response to T-dependent antigen [J].