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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Depletion of endogenous interleukin-10 augments interleukin-1 beta secretion by Mycobacterium bovis BCG-reactive human cells.
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Depletion of endogenous interleukin-10 augments interleukin-1 beta secretion by Mycobacterium bovis BCG-reactive human cells.

机译：内源性白介素10的耗竭会增加牛分枝杆菌BCG反应性人细胞对白介素1β的分泌。

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摘要

In this study, we found evidence that the interleukin-10 (IL-10) protein is functionally relevant in Mycobacterium bovis BCG-induced cytokine synthesis, as neutralization of endogenously synthesized IL-10 in human cells activated with BCG resulted in a two- to threefold increase in the level of IL-1 beta. When exogenous recombinant human IL-10 was added to human mononuclear cells, a significant reduction of BCG-induced IL-1 beta secretion was observed. This inhibitory effect was not attributed to a cytotoxic effect, since trypan blue exclusion studies indicated no loss of cell viability in the presence of IL-10, and it was specific, as it was completely abolished in the presence of anti-IL-10 neutralizing monoclonal antibody while an irrelevant antibody used as a control had no effect. Taken together, these are the first studies that demonstrate that the depletion of endogenous IL-10 via anti-IL-10 antibody results in a very significantly enhanced BCG-induced IL-1 beta secretion and that the addition of exogenous IL-10 to human mononuclear cells stimulated with BCG inhibits IL-1 beta production. Further experimental work is needed to determine if the neutralization of IL-10 activity via anti-IL-10 antibody indeed enhances cytokine synthesis in vivo. However, the present results may be of importance, since the use of anti-IL-10 antibody could presumably contribute to the protective immunity induced by BCG against tuberculosis via an increase in cytokine synthesis that would amplify antimicrobial systems.
机译：在这项研究中，我们发现有证据表明白介素10（IL-10）蛋白与牛分枝杆菌BCG诱导的细胞因子合成在功能上相关，因为中和内源性合成的IL-10在被BCG激活的人细胞中被中和。 IL-1β水平增加了三倍。当将外源重组人IL-10添加到人单核细胞中时，观察到BCG诱导的IL-1β分泌显着减少。该抑制作用不归因于细胞毒性作用，因为锥虫蓝排除研究表明在存在IL-10的情况下细胞活力没有损失，并且它是特异性的，因为在存在抗IL-10的中和作用下它被完全消除了。单克隆抗体，而无关的抗体用作对照则无效。综上所述，这些是第一个研究，证明通过抗IL-10抗体消耗内源性IL-10会导致BCG诱导的IL-1β分泌显着增强，并向人类增加外源性IL-10 BCG刺激的单核细胞抑制IL-1β的产生。需要进一步的实验工作以确定通过抗IL-10抗体中和IL-10活性是否确实增强了体内细胞因子的合成。但是，本研究结果可能很重要，因为使用抗IL-10抗体可能通过增加细胞因子合成来增加BCG诱导的针对肺结核的保护性免疫，从而增加抗菌系统。

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