Heat shock factor 1 suppresses the HIV-induced inflammatory response by inhibiting nuclear factor-κB
Heat shock factor 1 suppresses the HIV-induced inflammatory response by inhibiting nuclear factor-κB
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热休克因子 1 通过抑制核因子 kappa B 抑制 HIV 诱导的炎症反应
DOI：
10.1016/j.cellimm.2018.01.015
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发表时间：
2018-05-01
影响因子：
4.3
通讯作者：
Liu, Shuwen
中科院分区：
文献类型：
--
作者：
Pan, Xiaoyan;Lin, Jian;Liu, Shuwen
免疫应答紊乱加剧的持续性炎症被认为是淋巴组织中CD4(+)T细胞耗竭的主要原因，从而推动了艾滋病的发展。在这里，我们报告了热休克因子1(HSF1)作为一种先天抑制HIV诱导的炎症的作用。HSF1的激活被发现伴随着HIV感染过程中的炎症。进一步的研究发现，HSF1的激活抑制了HIV诱导的炎症。此外，HSF1过表达抑制了HIV引起的炎症反应，而HSF1缺乏则加剧了这种炎症反应。从机制上讲，HSF1与核因子-kappaB(NF-kappa B)在细胞核内竞争。总体而言，我们的报告强调HSF1是调节艾滋病毒引起的炎症的重要宿主因子，并可能成为治疗艾滋病的潜在靶点。
The persistent inflammation aggravated by a disordered immune response is considered to be the major cause of CD4(+) T cell depletion in lymphoid tissue, which impels the progression of AIDS. Here, we report that heat shock factor 1 (HSF1) works as an innate repressor of HIV-induced inflammation. The activation of HSF1 was found to accompany inflammation during HIV infection. Further research uncovered that HSF1 activation inhibited HIV-induced inflammation. In addition, HSF1 overexpression suppressed the inflammatory response induced by HIV, while HSF1 deficiency exacerbated that inflammation. Mechanistically, HSF1 was found to compete with nuclear factor-kappa B (NF-kappa B) in the nucleus. Generally, our report highlights that HSF1 is an important host factor in regulating HIV-induced inflammation and may work as a potential target for curing AIDS.