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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Regulatory T cells and chronic immune activation in human immunodeficiency virus 1 (HIV-1)-infected children.
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Regulatory T cells and chronic immune activation in human immunodeficiency virus 1 (HIV-1)-infected children.

机译:感染人类免疫缺陷病毒1(HIV-1)的儿童中的调节性T细胞和慢性免疫激活。

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The function of CD4(+) T cells with regulatory activity (T(regs)) is the down-regulation of immune responses. This suppressive activity may limit the magnitude of effector responses, resulting in failure to control human immunodeficiency virus 1 (HIV-1) infection, but may also suppress chronic immune activation, a characteristic feature of HIV-1 disease. We evaluated the correlation between viral load, immune activation and T(regs) in HIV-1-infected children. Eighty-nine HIV-1-infected children (aged 6-14 years) were included in the study and analysed for HIV-1 plasmaviraemia, HIV-1 DNA load, CD4 and CD8 cell subsets. T(reg) cells [CD4(+)CD25(high)CD127(low) forkhead box P3 (FoxP3(high))] and CD8-activated T cells (CD8(+)CD38(+)) were determined by flow cytometry. Results showed that the number of activated CD8(+)CD38(+)T cells increased in relation to HIV-1 RNA plasmaviraemia (r = 0.403, P < 0.0001). The proportion of T(regs) also correlated positively with HIV-1 plasmaviraemia (r = 0.323, P = 0.002), but correlated inversely with CD4(+) cells (r = -0.312, P = 0.004), thus suggesting a selective expansion along with increased viraemia and CD4(+) depletion. Interestingly, a positive correlation was found between the levels of T(regs) and CD8(+)CD38(+)T cells (r = 0.305, P = 0.005), and the percentage of T(regs) tended to correlate with HIV-1 DNA load (r = 0.224, P = 0.062). Overall, these findings suggest that immune activation contributes to the expansion of T(reg) cells. In turn, the suppressive activity of T(regs) may impair effector responses against HIV-1, but appears to be ineffective in limiting immune activation.
机译:具有调节活性(T(regs))的CD4(+)T细胞的功能是免疫反应的下调。这种抑制活性可能会限制效应子反应的幅度,导致无法控制人类免疫缺陷病毒1(HIV-1)感染,但也可能抑制慢性免疫激活,这是HIV-1疾病的特征。我们评估了HIV-1感染儿童的病毒载量,免疫激活和T(regs)之间的相关性。该研究包括89名HIV-1感染儿童(6-14岁),并分析了HIV-1血浆病毒血症,HIV-1 DNA载量,CD4和CD8细胞亚群。通过流式细胞术测定T(reg)细胞[CD4(+)CD25(高)CD127(低)前叉箱P3(FoxP3(高))和CD8激活的T细胞(CD8(+)CD38(+))。结果表明,活化的CD8(+)CD38(+)T细胞数量相对于HIV-1 RNA血浆病毒血症增加(r = 0.403,P <0.0001)。 T(regs)的比例也与HIV-1血浆病毒血症呈正相关(r = 0.323,P = 0.002),但与CD4(+)细胞呈负相关(r = -0.312,P = 0.004),因此表明选择性扩展以及病毒血症和CD4(+)耗竭增加。有趣的是,发现T(regs)与CD8(+)CD38(+)T细胞之间存在正相关(r = 0.305,P = 0.005),并且T(regs)的百分比倾向于与HIV- 1个DNA负载(r = 0.224,P = 0.062)。总体而言,这些发现表明免疫激活有助于T(reg)细胞的扩增。反过来,T(regs)的抑制活性可能会削弱效应器对HIV-1的反应,但似乎在限制免疫激活方面无效。

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