Smith Kelly D
Department of Pathology, University of Washington, Seattle, Washington 98195, USA.
Curr Opin Nephrol Hypertens. 2009 May;18(3):189-96. doi: 10.1097/MNH.0b013e32832a1d5f.
The innate immune system is our first line of defense against infection and injury, and responsible for initiating inflammatory and immune responses to resolve infections and repair injured tissues. This review focuses on the Toll-like receptors (TLRs) of the innate immune system and their role in recognizing infection and injury, and regulating inflammatory responses in the kidney.
There is increasing data to support a role for TLRs in immune complex-mediated glomerulonephritis. TLR7 has emerged as a key regulator of autoantibody production in murine lupus nephritis. In addition, studies have implicated TLR recognition of endogenous molecules released during cellular necrosis as critical regulators of sterile inflammation and injury. Tonic interactions between TLRs and environmental agonists derived from commensal microbes and endogenous sources may also influence autoimmune disease and inflammatory disorders affecting the kidney.
Future studies to decipher the contribution of TLRs and other innate immune receptors in the regulation of inflammation, immune responses, and injury in the kidney will pave the way for novel therapeutic interventions.
固有免疫系统是我们抵御感染和损伤的第一道防线,负责启动炎症和免疫反应以解决感染并修复受损组织。本综述聚焦于固有免疫系统的Toll样受体(TLR)及其在识别感染和损伤以及调节肾脏炎症反应中的作用。
越来越多的数据支持TLR在免疫复合物介导的肾小球肾炎中发挥作用。TLR7已成为小鼠狼疮性肾炎中自身抗体产生的关键调节因子。此外,研究表明TLR识别细胞坏死期间释放的内源性分子是无菌性炎症和损伤的关键调节因子。TLR与共生微生物和内源性来源的环境激动剂之间的持续相互作用也可能影响影响肾脏的自身免疫性疾病和炎症性疾病。
未来旨在破译TLR和其他固有免疫受体在调节肾脏炎症、免疫反应和损伤中的作用的研究将为新型治疗干预措施铺平道路。