The antiapoptotic protein Bcl-XL is dispensable for the development of effector and memory T lymphocytes
The antiapoptotic protein Bcl-XL is dispensable for the development of effector and memory T lymphocytes
复制标题
DOI：
10.4049/jimmunol.174.11.6967
复制
发表时间：
2005-06-01
影响因子：
4.4
通讯作者：
He, YW
中科院分区：
文献类型：
--
作者：
Zhang, N;He, YW
抗凋亡蛋白Bel-x(L)通过CD28、4-IBB和OX40的共刺激在活化的T淋巴细胞中诱导产生。Bcl-x(L)在记忆T淋巴细胞中也高度富集。基于这些证据，人们认为Bcl-x(L)在效应T淋巴细胞和记忆T淋巴细胞的产生中起着至关重要的作用。我们报道了T淋巴细胞中Bcl-x条件缺失的小鼠对单核细胞增生李斯特菌感染产生正常的CD8(+) T细胞反应。此外，Bcl-x条件敲除小鼠表现出正常的t依赖性体液免疫反应。这些结果表明，Bcl-x对于效应T淋巴细胞和记忆T淋巴细胞的产生是必不可少的，并且表明T淋巴细胞的共刺激是通过Bcl-x独立的机制促进其生存的。
The antiapoptotic protein Bel-x(L) is induced in activated T lymphocytes upon costimulation through CD28, 4-IBB, and OX40. Bcl-x(L) is also highly enriched in memory T lymphocytes. Based on this body of evidence, it was thought that Bcl-x(L) plays an essential role in the generation of effector and memory T lymphocytes. We report that mice with a conditional deletion of Bcl-x in T lymphocytes develop a normal CD8(+) T cell response to Listeria monocytogenes infection. Furthermore, Bcl-x conditional knockout mice exhibit normal T-dependent humoral immune responses. These results indicate that Bcl-x is dispensable for the generation of effector and memory T lymphocytes and suggest that costimulation of T lymphocytes promotes their survival through a Bcl-x, independent mechanism.