Mutations affecting either generation or survival of cells influence the pool size of mature B cells

被引：52

作者：

Rolink, AG

Brocker, T

Bluethmann, H

Kosco-Vilbois, MH

Andersson, J

Melchers, F

机构：

[1] Basel Inst Immunol, CH-4005 Basel, Switzerland

[2] Max Planck Inst Immunbiol, D-79108 Freiburg, Germany

[3] F Hoffmann La Roche & Co Ltd, Dept Roche Genet, CH-4070 Basel, Switzerland

[4] Serono Pharmaceut Res Inst, CH-1228 Plan Les Ouates, Switzerland

来源：

IMMUNITY | 1999年 / 10卷 / 05期

关键词：

D O I：

10.1016/S1074-7613(00)80061-8

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The mature B cell compartment of MHC class II-deficient B6 I-A alpha(-/-) and the btk-defective CBA/N mouse strain is 4- to 5-fold smaller than in wild-type B6 mice. The defect in B6 I-A alpha(-/-) mice is intrinsic to B cells and due to a 4- to 5-fold reduced lifespan, which however can be normalized by an I-E alpha(d) transgene, but only when expressed early during B cell development. The reduced number of mature B cells in the btk-defective CBA/N mouse is due to a 4- to 5-fold lower number of immature splenic B cells entering the mature compartment. The combined defects of reduced lifespan and impaired generation in double mutant mice result in a severe deficiency in the mature B cell pool.

引用

页码：619 / 628

页数：10

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