Mihara M, Moriya Y, Ohsugi Y
Fuji-Gotemba Research Laboratories, Chugai Pharmaceutical Co. Ltd., Shizuoka, Japan.
Int J Immunopharmacol. 1996 Jan;18(1):89-94. doi: 10.1016/0192-0561(95)00106-9.
A number of investigators has reported that there is increased production of interleukin-6 (IL-6) by fibroblasts and monocytes from the patients with systemic sclerosis (SS). However, the precise role of IL-6 in the pathogenesis of SS remains unclear. On the basis of our previous study showing that the complex of IL-6 and soluble IL-6 receptor (sIL-6R) could induce synovial fibroblast proliferation, we examined whether the IL-6-sL-6R complex could induce the proliferation of normal dermal fibroblastic cells (DF). IL-6 suppressed DF proliferation, and, in the presence of sIL-6R, dose-dependently showed much stronger suppressive effects on DF proliferation. This suppression was completely blocked by either anti-IL-6 or anti-sIL-6R antibody. Furthermore, the IL-6-sIL-6R complex significantly suppressed IL-1 beta-, TNF alpha- and PDGF-AA-induced DF proliferation. These lines of evidence suggest that the IL-6-sIL-6R complex may have potential as a useful agent for the treatment of SS.
一些研究人员报告称,系统性硬化症(SS)患者的成纤维细胞和单核细胞产生的白细胞介素-6(IL-6)有所增加。然而,IL-6在SS发病机制中的确切作用仍不清楚。基于我们之前的研究表明IL-6与可溶性IL-6受体(sIL-6R)的复合物可诱导滑膜成纤维细胞增殖,我们研究了IL-6-sL-6R复合物是否能诱导正常真皮成纤维细胞(DF)增殖。IL-6抑制DF增殖,并且在存在sIL-6R的情况下,剂量依赖性地对DF增殖表现出更强的抑制作用。这种抑制作用被抗IL-6或抗sIL-6R抗体完全阻断。此外,IL-6-sIL-6R复合物显著抑制IL-1β、TNFα和PDGF-AA诱导的DF增殖。这些证据表明,IL-6-sIL-6R复合物可能有潜力成为治疗SS的有用药物。