Bcl-2 rescues T lymphopoiesis in interleukin-7 receptor-deficient mice

被引:523
作者
Akashi, K
Kondo, M
vonFreedenJeffry, U
Murray, R
Weissman, IL
机构
[1] STANFORD UNIV,SCH MED,DEPT DEV BIOL,STANFORD,CA 94305
[2] DNAX RES INST MOL & CELLULAR BIOL INC,DEPT IMMUNOL,PALO ALTO,CA 94304
关键词
D O I
10.1016/S0092-8674(00)80291-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mice lacking functional IL-7 or lL-7R alpha genes are severely deficient in developing thymocytes, T cells, and B cells. IL-7 and IL-7 receptor functions are believed to result in lymphoid cell proliferation and cell maturation, implying signal transduction pathways directly involved in mitogenesis and elaboration of developmentally specific new gene programs. Here, we show that enforced expression of the bcl-2 gene in T-lymphoid cells (by crossing in the E mu-bcl-2 transgene) in IL-7R alpha-deficient mice results in a significant restoration of thymic positive selection and T cell numbers and function. We propose cell survival signals to be the principal function of IL-7R engagement in thymic and T cell development.
引用
收藏
页码:1033 / 1041
页数:9
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