通过调节 TLR 信号抑制炎症。
DAMPening inflammation by modulating TLR signalling.
机构信息
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, 65 Aspenlea Road, Hammersmith, London W6 8LH, UK.
出版信息
Mediators Inflamm. 2010;2010. doi: 10.1155/2010/672395. Epub 2010 Jul 13.
Damage-associated molecular patterns (DAMPs) include endogenous intracellular molecules released by activated or necrotic cells and extracellular matrix (ECM) molecules that are upregulated upon injury or degraded following tissue damage. DAMPs are vital danger signals that alert our immune system to tissue damage upon both infectious and sterile insult. DAMP activation of Toll-like receptors (TLRs) induces inflammatory gene expression to mediate tissue repair. However, DAMPs have also been implicated in diseases where excessive inflammation plays a key role in pathogenesis, including rheumatoid arthritis (RA), cancer, and atherosclerosis. TLR activation by DAMPs may initiate positive feedback loops where increasing tissue damage perpetuates pro-inflammatory responses leading to chronic inflammation. Here we explore the current knowledge about distinct signalling cascades resulting from self TLR activation. We also discuss the involvement of endogenous TLR activators in disease and highlight how specifically targeting DAMPs may yield therapies that do not globally suppress the immune system.
损伤相关分子模式(DAMPs)包括由激活或坏死细胞释放的内源性细胞内分子和细胞外基质(ECM)分子,这些分子在损伤或组织损伤后降解时会被上调。DAMPs 是重要的危险信号,可在感染和无菌性损伤时提醒我们的免疫系统注意组织损伤。DAMP 激活 Toll 样受体(TLR)可诱导炎症基因表达,从而介导组织修复。然而,DAMPs 也与过度炎症在发病机制中起关键作用的疾病有关,包括类风湿关节炎(RA)、癌症和动脉粥样硬化。DAMP 对 TLR 的激活可能引发正反馈循环,其中增加的组织损伤使促炎反应持续存在,导致慢性炎症。在这里,我们探讨了关于自身 TLR 激活产生的不同信号级联的现有知识。我们还讨论了内源性 TLR 激活物在疾病中的作用,并强调了如何特异性靶向 DAMPs 可能产生不会全面抑制免疫系统的治疗方法。
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