OX40 promotes Bcl-xL and Bcl-2 expression and is essential for long-term survival of CD4 T cells
OX40 promotes Bcl-xL and Bcl-2 expression and is essential for long-term survival of CD4 T cells
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DOI：
10.1016/s1074-7613(01)00191-1
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发表时间：
2001-09-01
期刊：
影响因子：
32.4
通讯作者：
Croft, M
中科院分区：
文献类型：
--
作者：
Rogers, PR;Song, JX;Croft, M
重要的是要了解哪些分子对长期免疫至关重要。我们表明，OX 40（CD 134）与CD 28是必需的CD 4 T细胞抗原驱动的扩增后的生存。与早期表现出缺陷的CD 28（-/-）T细胞相反，OX 40（-/-）T细胞在IL-2产生、细胞分裂和扩增方面相对不受损害。然而，OX 40（-/-）T细胞在活化后4-8天下降以维持高水平的Bci-xL和Bcl-2，并经历凋亡。相反，OX 40刺激促进Bcl-xL和Bcl-2并抑制细胞凋亡。此外，用Bcl-xL或Bcl-2逆转录病毒转导OX 40（-/-）T细胞逆转其存活缺陷。因此，CD 28和OX 40之间存在时间关系，OX 40是抗原驱动的T细胞存活的关键调节因子。
It is important to understand which molecules are essential for long-lived immunity. We show that OX40 (CD134) is required with CD28 for the survival of CD4 T cells following antigen-driven expansion. In contrast to CD28(-/-) T cells, which show defects early, OX40(-/-)T cells are relatively unimpaired in IL-2 production, cell division, and expansion. However, OX40(-/-) T cells fall to maintain high levels of Bci-xL and Bcl-2 4-8 days after activation, and undergo apoptosis. Conversely, OX40 stimulation promotes Bcl-xL and Bcl-2 and suppresses apoptosis. Moreover, retroviral transduction of OX40(-/-) T cells with Bcl-xL or Bcl-2 reverses their survival defect. Thus, a temporal relationship exists between CD28 and OX40, with OX40 being a critical regulator of antigen-driven T cell survival.