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首页> 美国卫生研究院文献>other >Deficient IL-2 Produced by Activated CD56+ T Cells Contributes to Impaired NK Cell-Mediated ADCC Function in Chronic HIV-1 Infection
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Deficient IL-2 Produced by Activated CD56+ T Cells Contributes to Impaired NK Cell-Mediated ADCC Function in Chronic HIV-1 Infection

机译：活化的CD56 + T细胞产生的不足的IL-2导致受损的NK细胞介导的ADCC在慢性HIV-1感染中的功能。

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>Background: Antibody-dependent cellular cytotoxicity (ADCC), which mainly mediated by natural killer (NK) cells, may play a critical role in human immunodeficiency virus type-1 (HIV-1) disease progression. However, the potential mechanisms that affecting NK-mediated ADCC response are still not well-elucidated.>Methods: Antigen-antibody complex model of Ab-opsonized P815 cells was adopted to induce a typical non-specific ADCC response. The capacities of HIV-1 specific NK-ADCC were measured by using the combination model of gp120 protein and plasma of HIV-1 elite controllers. The levels of plasma cytokine were measured by ELISA. Anti-IL-2 blocking antibody was used to analyze the impact of activated CD56+ T cells on NK-ADCC response.>Results: IL-2, IL-15, IFN-α, and IFN-β could effectively enhance the non-specific and HIV-1-specific NK-ADCC responses. Compared with healthy controls, HIV-1-infected patients showed decreased plasma IL-2 levels, while no differences of plasma IFN-α, IL-15, and IFN-β were presented. IL-2 production was detected from CD56+ T cells activated through antibody-dependent manner. The capability of NK-ADCC could be weakened by blocking IL-2 secretion from activated CD56+ T cells. Although no difference of frequencies of CD56+ T cells was found between HIV-1-infected patients and healthy controls, deficient IL-2 secretion from activated CD56+ T were found in chronic HIV-1 infection.>Conclusions: The impaired ability of activated CD56+ T cells to secreting IL-2 might contribute to the attenuated NK cell-mediated ADCC function in HIV-1 infection.
机译：>背景：主要由自然杀伤（NK）细胞介导的抗体依赖性细胞毒性（ADCC）在人类1型免疫缺陷病毒（HIV-1）疾病进展中可能起关键作用。然而，仍未充分阐明影响NK介导的ADCC反应的潜在机制。>方法：采用Ab-调理过的P815细胞抗原-抗体复合物模型诱导典型的非特异性ADCC反应。通过使用gp120蛋白和HIV-1精英控制者血浆的组合模型测量HIV-1特异性NK-ADCC的能力。通过ELISA测量血浆细胞因子的水平。使用抗IL-2阻断抗体来分析活化的CD56 + T细胞对NK-ADCC应答的影响。>结果： IL-2，IL-15，IFN -α和IFN-β可以有效增强非特异性和HIV-1特异性NK-ADCC反应。与健康对照组相比，感染HIV-1的患者血浆IL-2水平降低，而血浆IFN-α，IL-15和IFN-β没有差异。从以抗体依赖性方式激活的CD56 + T细胞中检测到IL-2的产生。阻断活化的CD56 + T细胞的IL-2分泌可削弱NK-ADCC的能力。尽管在感染HIV-1的患者和健康对照组之间未发现CD56 + T细胞的频率差异，但在激活的CD56 + T中发现了IL-2分泌不足。慢性HIV-1感染。>结论：活化的CD56 + T细胞分泌IL-2的能力受损可能导致NK细胞介导的ADCC功能减弱。 1感染。

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