Williams Lynn, Jarai Gabor, Smith Alexandra, Finan Peter
Kennedy Institute of Rheumatology, London, United Kingdom.
J Leukoc Biol. 2002 Oct;72(4):800-9.
Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine with numerous immunomodulatory effects, including the inhibition of proinflammatory cytokine production. The mechanisms by which IL-10 exerts these effects still remain largely unknown. As there is evidence that suggests IL-10-mediated cytokine suppression requires the induction of an intermediate gene, we have used gene-chip technology to identify IL-10-inducible genes in human monocytes. We have been able to identify a total of 19 genes that are up-regulated in response to IL-10. Three of these genes had been identified previously: IL-1ra, suppressors of cytokine signaling-3, and CD163; however, the other 16 represent newly identified IL-10-responsive genes. Further analysis of the regulation of eight of these genes showed a remarkable specificity to regulation by lipopolysaccharides (LPS) and IL-10, but not by other anti-inflammatory mediators such as IL-4 and transforming growth factor-beta, suggesting that two diverse stimuli such as IL-10 and LPS may engage common signaling mechanisms.
白细胞介素-10（IL-10）是一种具有多种免疫调节作用的强效抗炎细胞因子，包括抑制促炎细胞因子的产生。IL-10发挥这些作用的机制在很大程度上仍不清楚。由于有证据表明IL-10介导的细胞因子抑制需要诱导一个中间基因，我们利用基因芯片技术在人单核细胞中鉴定IL-10诱导基因。我们总共鉴定出19个因IL-10而上调的基因。其中三个基因先前已被鉴定：IL-1ra、细胞因子信号转导抑制因子-3和CD163；然而，其他16个代表新鉴定的IL-10应答基因。对其中八个基因调控的进一步分析显示，它们对脂多糖（LPS）和IL-10的调控具有显著特异性，但对其他抗炎介质如IL-4和转化生长因子-β则无此特性，这表明IL-10和LPS等两种不同的刺激可能采用共同的信号传导机制。
