CD30 induction of human immunodeficiency virus gene transcription is mediated by TRAF2.
CD30 induction of human immunodeficiency virus gene transcription is mediated by TRAF2.
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CD30 诱导人类免疫缺陷病毒基因转录是由 TRAF2 介导的。
DOI：
10.1073/pnas.94.4.1390
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发表时间：
1997
影响因子：
11.1
通讯作者：
Geha,RS
中科院分区：
文献类型：
--
作者：
Tsitsikov,EN;Wright,DA;Geha,RS
CD30是肿瘤坏死因子受体(TNFR)超家族成员，表达于活化的T、B淋巴细胞和自然杀伤细胞上。先前研究表明，CD30的结扎可以诱导慢性感染T淋巴细胞中的NF-κB活化和HIV的表达。在这项研究中，我们报道了TNFR相关因子(TRAF)家族的两个成员，TRAF1和TRAF2，独立地与CD30(CD30IC)的胞内结构域结合。瞬时过表达TRAF2，而不是TRAF1，在T细胞系KT3中诱导了NF-κB的激活和HIV-1长末端重复序列驱动的转录。此外，由TRAF1和TRAF2的TRAF结构域组成的显性负性突变体抑制了CD30对NF-κB激活和HIV-1转录的诱导。这些结果提示，CD30的结扎可能通过TRAF-2介导的NF-κB的激活来增强HIV的表达。
CD30 is a member of the tumor necrosis factor receptor (TNFR) superfamily expressed on activated T and B lymphocytes and natural killer cells. Ligation of CD30 was previously shown to induce NF-κB activation and HIV expression in chronically infected T lymphocytes. In this study, we report that two members of the TNFR-associated factor (TRAF) family of proteins, TRAF1 and TRAF2, independently bind to the intracellular domain of CD30 (CD30IC). Transient overexpression of TRAF2, but not TRAF1, induced NF-κB activation and HIV-1-long terminal repeat-driven transcription in the T cell line, KT3. Moreover, dominant negative mutants consisting of the TRAF domain of TRAF1 and TRAF2 inhibited CD30 induction of NF-κB activation and HIV-1 transcription. These results suggest that CD30 ligation may enhance the expression of HIV via TRAF-2-mediated activation of NF-κB.