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首页> 外文期刊>Cellular immunology >Use of the anti-inflammatory cytokine interleukin-11 to reverse HIV-1gp120 repression of a natural killer cell line
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Use of the anti-inflammatory cytokine interleukin-11 to reverse HIV-1gp120 repression of a natural killer cell line

机译:抗炎细胞因子白介素11逆转HIV-1gp120对自然杀伤细胞系的抑制作用

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Enhancing natural killer (NK) cell activation has been associated with protection from human immunodeficiency virus-1 (HIV-1) infections and slowed onset of immunodeficiency. However, soluble HIV-1 envelope protein, gp120, has been shown to impair NK cell cytokine secretion and cell-mediated cytotoxicity. Here we show that gp120 suppressed IFN-γ production and cytotoxic function of a human NK cell line NK-92MI. We furthermore demonstrated that an anti-inflammatory cytokine interleukin-11 can restore effector functions to repressed NK-92MI cells. These studies support the notion that IL-11 administration may reduce HIV-1-mediated immune activation and exhaustion while achieving elimination of virally-infected cells through restored NK cell function.
机译:增强自然杀伤(NK)细胞活化与保护免受人类免疫缺陷病毒1(HIV-1)感染和减缓免疫缺陷发作有关。但是,已显示可溶性HIV-1包膜蛋白gp120会损害NK细胞的细胞因子分泌和细胞介导的细胞毒性。在这里,我们显示gp120抑制人NK细胞系NK-92MI的IFN-γ产生和细胞毒性功能。我们进一步证明抗炎细胞因子白介素11可以恢复效应器功能,以抑制NK-92MI细胞。这些研究支持以下观点:IL-11给药可以减少HIV-1介导的免疫激活和疲劳,同时通过恢复的NK细胞功能消除病毒感染的细胞。

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