Bcl-2 rescues T lymphopoiesis in interleukin-7 receptor-deficient mice
Bcl-2 rescues T lymphopoiesis in interleukin-7 receptor-deficient mice
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DOI：
10.1016/s0092-8674(00)80291-3
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发表时间：
1997-06-27
期刊：
影响因子：
64.5
通讯作者：
Weissman, IL
中科院分区：
文献类型：
--
作者：
Akashi, K;Kondo, M;Weissman, IL
缺乏功能性IL-7或IL-7 R α基因的小鼠在发育胸腺细胞、T细胞和B细胞方面严重缺陷。IL-7和IL-7受体功能被认为导致淋巴样细胞增殖和细胞成熟，这意味着信号转导途径直接参与有丝分裂和发育特异性新基因程序的阐述。在这里，我们表明，在T淋巴细胞中的bcl-2基因的强制表达（通过在E mu-bcl-2转基因交叉）在IL-7 R α缺陷小鼠的胸腺阳性选择和T细胞的数量和功能的显着恢复。我们提出细胞存活信号是IL-7 R参与胸腺和T细胞发育的主要功能。
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.