Critical synergy of CD30 and OX40 signals in CD4 T cell Homeostasis and Th1 immunity to Salmonella
Critical synergy of CD30 and OX40 signals in CD4 T cell Homeostasis and Th1 immunity to Salmonella
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DOI：
10.4049/jimmunol.180.5.2824
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发表时间：
2008-03-01
影响因子：
4.4
通讯作者：
Cunningham, Adam F.
中科院分区：
文献类型：
--
作者：
Gaspal, Fabrina;Bekiaris, Vasileios;Cunningham, Adam F.
CD30和OX40（CD134）是TNFR超家族的成员，在活化的CD4 T细胞上表达，并且这两种分子缺陷的小鼠在建立CD4 T细胞依赖性记忆Ab应答的能力上具有显著缺陷。这篇文章表明，这些小鼠也未能控制沙门氏菌感染，因为CD30和OX40信号都是生存所需的，但不是CD4 Th1细胞的承诺。这些信号也是在淋巴细胞减少环境中活化的CD4 T细胞存活所需的。最后，沙门氏菌和淋巴细胞减少症显示出协同作用，选择性地消耗缺乏OX40和CD30的CD4 T细胞。总的来说，这些发现确定了一种新的机制，Th1反应是持续的。
CD30 and OX40 (CD134) are members of the TNFR superfamily expressed on activated CD4 T cells, and mice deficient in both these molecules harbor a striking defect in the capacity to mount CD4 T cell-dependent memory Ab responses. This article shows that these mice also fail to control Salmonella infection because both CD30 and OX40 signals are required for the survival but not commitment of CD4 Th1 cells. These signals are also needed for the survival of CD4 T cells activated in a lymphopenic environment. Finally, Salmonella and lymphopenia are shown to act synergistically in selectively depleting CD4 T cells deficient in OX40 and CD30. Collectively these findings identify a novel mechanism by which Th1 responses are sustained.