Seitz M, Loetscher P, Dewald B, Towbin H, Gallati H, Baggiolini M
Division of Rheumatology, University Hospital, Bern, Switzerland.
Eur J Immunol. 1995 Apr;25(4):1129-32. doi: 10.1002/eji.1830250443.
In this study we have examined the effects of interleukin-10 (IL-10) on blood mononuclear cells (MNC) and on skin as well as on synovial fibroblasts. In unstimulated MNC, we found that IL-10 is a potent stimulator of interleukin-1 receptor antagonist (IL-1ra) and monocyte chemoattractant protein-1 (MCP-1) production and an inhibitor of IL-8 release. In cells exposed to IL-1 beta, it also moderately stimulated IL-1ra production and release of soluble tumor necrosis factor receptor p75 (sTNF-R p75) and inhibited IL-8 and MCP-1 production. In addition, we have evidence that the biological effects of IL-10 are not restricted to hematopoietic cells. IL-10 stimulated sTNF-R p55 dose-dependently and inhibited MCP-1 release from IL-1 beta-activated fibroblasts, whereas IL-8 production was not affected. Taken together, these findings identify novel biological actions of IL-10 on blood mononuclear and connective tissue cells which support its regulatory functions as a suppressor of inflammatory processes.
在本研究中，我们检测了白细胞介素-10（IL-10）对血液单核细胞（MNC）、皮肤以及滑膜成纤维细胞的影响。在未受刺激的MNC中，我们发现IL-10是白细胞介素-1受体拮抗剂（IL-1ra）和单核细胞趋化蛋白-1（MCP-1）产生的强效刺激剂，也是IL-8释放的抑制剂。在暴露于IL-1β的细胞中，它还适度刺激IL-1ra的产生以及可溶性肿瘤坏死因子受体p75（sTNF-R p75）的释放，并抑制IL-8和MCP-1的产生。此外，我们有证据表明IL-10的生物学效应并不局限于造血细胞。IL-10剂量依赖性地刺激sTNF-R p55，并抑制IL-1β激活的成纤维细胞释放MCP-1，而IL-8的产生未受影响。综上所述，这些发现确定了IL-10对血液单核细胞和结缔组织细胞的新生物学作用，这支持了其作为炎症过程抑制剂的调节功能。
