The tragic fate of group 3 innate lymphoid cells during HIV-1 infection.
The tragic fate of group 3 innate lymphoid cells during HIV-1 infection.
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HIV-1 感染期间第 3 组先天淋巴细胞的悲惨命运。
DOI：
10.1172/jci83823
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发表时间：
2015
期刊：
影响因子：
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通讯作者：
Fu,Yang-Xin
中科院分区：
文献类型：
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作者：
Guo,Xiaohuan;Fu,Yang-Xin
HIV-1感染通常导致与肠道微生物易位相关的全身性慢性炎症。最近定义的第3组先天淋巴样细胞（ILC 3）是维持肠道屏障功能的关键;然而，目前尚不清楚HIV-1感染是否以及如何影响这些细胞的功能。在本期的JCI中，Zhang及其同事提出了令人信服的证据，证明ILC 3的存活和功能受到HIV-1感染的严重损害。作者提供的证据表明，HIV-1感染诱导浆细胞样树突状细胞（pDC）的持续活化和I型IFN的产生，它们共同增加ILC 3上死亡受体CD 95的表达，从而促进随后的ILC 3凋亡。总之，这些结果确定了一种机制，解释了肠屏障功能受损，导致慢性HIV-1感染，并阐明了pDC在HIV-1免疫发病机制和治疗中的作用。
HIV-1 infection usually leads to systemic chronic inflammation that is associated with gut microbial translocation. The recently defined group 3 innate lymphoid cells (ILC3s) are critical for maintenance of intestinal barrier function; however, it is not clear whether and how HIV-1 infection influences the function of these cells. In this issue of theJCI, Zhang and colleagues present compelling evidence that the survival and function of ILC3s are dramatically impaired by HIV-1 infection. The authors provide evidence that HIV-1 infection induces persistent activation of plasmacytoid dendritic cells (pDCs) and production of type I IFNs, which together increase expression of death receptor CD95 on ILC3s and thereby promote subsequent ILC3 apoptosis. Together, these results identify a mechanism that explains the impaired intestinal barrier function that results from chronic HIV-1 infection and shed light on the role of pDCs in HIV-1 immunopathogenesis and therapy.