Malemud Charles J, Meszaros Evan C, Wylie Meredith A, Dahoud Wissam, Skomorovska-Prokvolit Yelenna, Mesiano Sam
Department of Medicine, Division of Rheumatic Diseases, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106, USA.
Department of Reproductive Biology, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106, USA; Department of Pathology, Institute of Pathology, Case Western Reserve University, School of Medicine, University Hospitals Case Medical Center, Cleveland, Ohio 44106, USA.
J Clin Cell Immunol. 2016 Jun;7(3). doi: 10.4172/2155-9899.1000422. Epub 2016 Jun 3.
We reported at the Keynote Forum of Immunology Summit-2015 that recombinant human (rh) TNF-α or rhIL-6 stimulated production of matrix metalloproteinase-9 (MMP-9) in the T/C28a2 and C-28/I2 human immortalized chondrocyte cell lines. Furthermore, we reported that tocilizumab (TCZ), a fully humanized monoclonal antibody which neutralizes IL-6-mediated signaling, inhibited the rhIL-6-mediated increase in the production of MMP-9. IL-6 is also a known activator of the JAK/STAT signaling pathway. In that regard, we evaluated the effect of rhIL-6 on total and phosphorylated Signal Transducer and Activator of Transcription by these chondrocyte lines which showed that whereas STAT3 was constitutively phosphorylated in T/C28a2 chondrocytes, rhIL-6 activated STAT3 in C-28/I2 chondrocytes. The finding that rhIL-6 increased the production of MMP-9 by human immortalized chondrocyte cell lines may have important implications with respect to the destruction of articular cartilage in rheumatoid arthritis and osteoarthritis. Thus, the markedly elevated level of IL-6 in rheumatoid arthritis and osteoarthritis sera and synovial fluid would be expected to generate significant MMP-9 to cause the degradation of articular cartilage extracellular matrix proteins. The finding that TCZ suppressed rhIL-6-mediated MMP-9 production suggests that TCZ, currently employed in the medical therapy of rheumatoid arthritis, could be considered as a drug for osteoarthritis.
我们在2015年免疫学峰会的主题论坛上报告称,重组人(rh)肿瘤坏死因子-α(TNF-α)或rh白细胞介素-6(IL-6)可刺激T/C28a2和C-28/I2人永生化软骨细胞系中基质金属蛋白酶-9(MMP-9)的产生。此外,我们还报告称,托珠单抗(TCZ),一种可中和IL-6介导信号传导的全人源化单克隆抗体,可抑制rhIL-6介导的MMP-9产生增加。IL-6也是已知的JAK/STAT信号通路激活剂。在这方面,我们评估了rhIL-6对这些软骨细胞系中总信号转导和转录激活因子以及磷酸化信号转导和转录激活因子的影响,结果表明,虽然STAT3在T/C28a2软骨细胞中组成性磷酸化,但rhIL-6可激活C-28/I2软骨细胞中的STAT3。rhIL-6可增加人永生化软骨细胞系中MMP-9的产生这一发现,可能对类风湿性关节炎和骨关节炎中关节软骨的破坏具有重要意义。因此,类风湿性关节炎和骨关节炎血清及滑液中IL-6水平的显著升高,预计会产生大量MMP-9,导致关节软骨细胞外基质蛋白的降解。TCZ可抑制rhIL-6介导的MMP-9产生这一发现表明,目前用于类风湿性关节炎医学治疗的TCZ,可被视为一种治疗骨关节炎的药物。