Inhibitory effect of interleukin-10 on human leukocyte interferon-alpha production by Sendai virus.

X X Zhao, M J Liao, A Rashidbaigi
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Abstract

Treatment of human peripheral blood leukocytes (hPBL) with Sendai virus induces significant production of human interferon-alpha (IFN-alpha). Addition of human recombinant interleukin-10 (IL-10) to hPBL in vitro prior to treatment with Sendai virus resulted in considerable inhibition of IFN-alpha production. Downregulation of IFN-alpha production was IL-10 concentration-dependent and observed at IL-10 concentrations of as low as 0.05 ng/ml, with a median effective dose (ED50) of about 5 ng/ml. Inhibition of IFN-alpha production by IL-10 occurred at an early stage of Sendai virus induction. The inhibitory effect of IL-10 on leukocyte interferon production was specific and blocked by pretreatment with neutralizing polyclonal anti-IL-10 antibody. This downregulatory effect is at the transcriptional level, since IL-10 inhibits IFN-alpha mRNA accumulation upon Sendai virus treatment. These data suggest that leukocyte IFN-alpha production is a highly regulated process that is modulated by cytokines such as IL-10 during early immunological response to infection.

白细胞介素-10对仙台病毒产生人白细胞干扰素- α的抑制作用
用仙台病毒治疗人外周血白细胞(hPBL)可诱导人干扰素- α (ifn - α)的显著产生。在体外用仙台病毒治疗hPBL之前,将人重组白细胞介素-10 (IL-10)添加到hPBL中,可显著抑制ifn - α的产生。ifn - α产生的下调与IL-10浓度有关,IL-10浓度低至0.05 ng/ml,中位有效剂量(ED50)约为5 ng/ml。在仙台病毒诱导的早期,IL-10抑制了ifn - α的产生。IL-10对白细胞干扰素产生的抑制作用是特异性的,并通过中和性多克隆抗IL-10抗体预处理阻断。这种下调作用是在转录水平上,因为IL-10抑制仙台病毒处理时ifn - α mRNA的积累。这些数据表明,白细胞ifn - α的产生是一个高度调控的过程,在感染的早期免疫反应中由细胞因子如IL-10调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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