3, 进而参与关节骨及软骨的破坏。TWEAK诱导FLS合成MMPs的具体机制尚不完全清楚, 考虑是与其受体结合, 激活下游的信号转导分子而发挥作用[8]。至于TWEAK诱导FLS合成MMP3的过程中激活了哪些信号转导分子, TNFα和IL1β协同TWEAK诱导FLS合成MMP3的相关机制, 尚需进一步的实验研究。因此, 我们推测TWEAK作为一种新的致关节炎的介质, 能够刺激FLS合成MMP3直接损伤关节骨和软骨, 导致RA的发生和发展, 阻断TWEAK的作用可能成为RA治疗的新策略[9]。
【参考文献】 [1] Huber LC, Distler O, Tarner I, et al. Synovial fibroblasts; keyplayers in rheumatoid arthritis[J]. Rheumatology (Oxford), 2006, 45(6): 669-675. [2] Chicheportiche Y, Chicheportiche R, Sizing I, et al. Proinflammatory activity of TWEAK on human dermal fibroblasts and synoviocytes: blocking and enhancing effects of antiTWEAK monoclonal antibodies[J]. Arthritis Res, 2002, 4(2): 126-133.
[3] Kamijo S, Nakajima A, Kamata K, et al. Involvement of TWEAK/Fn14 interaction in the synovial inflammation of RA[J]. Rheumatology (Oxford), 2008, 47(4): 442-450.
[4] Rannou F, Franois M, Corvol MT, et al. Cartilage breakdown in rheumatoid arthritis[J]. Joint Bone Spine, 2006, 上一页 [1] [2] [3] [4] [5] [6] [7] [8] [9] 下一页 |