Gravestein L A, Amsen D, Boes M, Calvo C R, Kruisbeek A M, Borst J
Division of Cellular Biochemistry, The Netherlands Cancer Institute, Amsterdam.
Eur J Immunol. 1998 Jul;28(7):2208-16. doi: 10.1002/(SICI)1521-4141(199807)28:07<2208::AID-IMMU2208>3.0.CO;2-L.
CD27 is a lymphocyte-specific member of the TNF receptor (TNFR) family. It is a costimulatory molecule for peripheral T cells, as defined by its ability to enhance the TCR-induced proliferative response. We show here that CD27 augments TCR-induced Jun N-terminal kinase (JNK) activity in primary murine lymph node T cells. To investigate how CD27 couples to JNK, we performed a yeast two hybrid screen with the CD27 cytoplasmic tail. This revealed that CD27 directly associates with Traf-2. Transfection experiments using dominant negative Traf-2 indicated that CD27 communicates with JNK via Traf-2. These findings group CD27 together with other members of the TNFR family, TNFR-1, -2, CD30 and CD40, which have all been shown to couple to Traf proteins. Since Traf proteins have been reported to initiate an anti-apoptotic signaling pathway, our data suggest that CD27 not only regulates proliferation, but also survival of T lymphocytes.
CD27是肿瘤坏死因子受体（TNFR）家族中的淋巴细胞特异性成员。它是外周T细胞的共刺激分子，其增强TCR诱导的增殖反应的能力可对此进行定义。我们在此表明，CD27可增强原代小鼠淋巴结T细胞中TCR诱导的Jun N末端激酶（JNK）活性。为了研究CD27如何与JNK偶联，我们用CD27细胞质尾进行了酵母双杂交筛选。这表明CD27直接与Traf-2相关联。使用显性负性Traf-2的转染实验表明，CD27通过Traf-2与JNK进行通信。这些发现将CD27与TNFR家族的其他成员TNFR-1、-2、CD30和CD40归为一组，所有这些成员均已被证明可与Traf蛋白偶联。由于据报道Traf蛋白可启动抗凋亡信号通路，我们的数据表明CD27不仅调节T淋巴细胞的增殖，还调节其存活。
