首页> 外文期刊>Blood: The Journal of the American Society of Hematology >Lack of endogenous TRIM5alpha-mediated restriction in rhesus macaque dendritic cells.
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Lack of endogenous TRIM5alpha-mediated restriction in rhesus macaque dendritic cells.

机译:恒河猴猕猴树突状细胞缺乏内源性TRIM5alpha介导的限制。

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摘要

Rhesus macaques are resistant to infection by HIV-1 as a result of an innate cellular restriction mechanism attributable to the expression of rhTRIM5alpha, a member of the large tripartite motif (TRIM) protein family. TRIM5alpha-mediated restriction, which occurs before reverse transcription through targeting of the HIV-1 capsid, has been identified in a number of macaque primary cells and cell lines and is thought to occur in all macaque cell types. We report, however, that rhesus macaque dendritic cells (DCs) lack TRIM5alpha-mediated restriction and are equally permissive to HIV-1 infection as human DCs. Evidence suggests that, although TRIM5alpha RNA levels are normal in these cells, the protein may be dysfunctional. We propose that abrogation of TRIM5alpha-mediated restriction in DCs, although still operative in cells that replicate HIV-1 (macrophages, T lymphocytes), illustrates the need for innate mechanisms to not inhibit adaptive immune responses to ensure an optimal fight against pathogens.
机译:恒河猴对HIV-1具有抗性,这是由于固有的细胞限制机制所致,该机制归因于rhTRIM5alpha(大的三方基序(TRIM)蛋白家族的成员)的表达。 TRIM5alpha介导的限制发生在通过靶向HIV-1衣壳进行逆转录之前,已经在许多猕猴原代细胞和细胞系中得到鉴定,并且被认为发生在所有猕猴细胞类型中。我们报告,但是,恒河猴猕猴树突状细胞(DCs)缺乏TRIM5alpha介导的限制,并且与人类DCs一样同样允许HIV-1感染。有证据表明,尽管在这些细胞中TRIM5alpha RNA水平正常,但该蛋白可能功能失调。我们建议废除DCS中的TRIM5alpha介导的限制,尽管仍然在复制HIV-1的细胞(巨噬细胞,T淋巴细胞)中起作用,这说明需要先天机制不抑制适应性免疫反应以确保最佳对抗病原体。

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