Innate immunity sensors participating in pathophysiology of joint diseases: a brief overview.
Innate immunity sensors participating in pathophysiology of joint diseases: a brief overview.
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DOI：
10.1615/jlongtermeffmedimplants.2014010825
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发表时间：
2014
影响因子：
--
通讯作者：
Goodman SB
中科院分区：
文献类型：
--
作者：
Gallo J;Raska M;Konttinen YT;Nich C;Goodman SB
先天免疫系统由功能专门的“模块”组成，这些“模块”通过位于组织细胞表面或内部的传感器响应一组特定的刺激而被激活。这些细胞筛选组织中各种外源性和内源性危险/损伤诱导的信号，目的是拒绝或耐受它们并保持组织完整性。按照这个思路，炎症进化为恢复组织稳态的适应性工具。许多疾病是由先天免疫反应的适应不良介导的，导致慢性炎症和组织损伤持续存在。在这里，我们回顾了有关先天免疫传感器与类风湿关节炎、骨关节炎和全关节置换术无菌性松动的发展之间相互影响的最新证据。关于后一个主题，越来越多的证据表明，无菌性松动和假体周围骨溶解是由于假体周围组织对人工关节不断释放的副产物的长期适应不良造成的。
The innate immune system consists of functionally specialized “modules” that are activated in response to a particular set of stimuli via sensors located on the surface or inside the tissue cells. These cells screen tissues for a wide range of exogenous and endogenous danger/damage-induced signals with the aim to reject or tolerate them and maintain tissue integrity. In this line of thinking, inflammation evolved as an adaptive tool for restoring tissue homeostasis. A number of diseases are mediated by a maladaptation of the innate immune response, perpetuating chronic inflammation and tissue damage. Here, we review recent evidence on the cross talk between innate immune sensors and development of rheumatoid arthritis, osteoarthritis, and aseptic loosening of total joint replacements. In relation to the latter topic, there is a growing body of evidence that aseptic loosening and periprosthetic osteolysis results from long-term maladaptation of periprosthetic tissues to the presence of by-products continuously released from an artificial joint.