Immunopathogenesis of osteoarthritis.

Immunopathogenesis of osteoarthritis.
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DOI:
10.1016/j.clim.2012.12.011
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发表时间:
2013-03
期刊:
Clinical immunology (Orlando, Fla.)
影响因子:
--
通讯作者:
Haqqi TM
Haqqi TM
中科院分区:
其他
文献类型:
--
作者:
Haseeb A;Haqqi TM

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尽管骨关节炎(OA)主要被认为是关节软骨的退化性疾病,但越来越多的数据表明免疫系统所有分支都参与其中。遗传、代谢或机械因素会对软骨造成初步损伤,导致多种软骨特异性自身抗原的释放,从而触发免疫反应的激活。 T细胞、B细胞和巨噬细胞等免疫细胞浸润关节组织,关节内不同种类的细胞释放细胞因子和趋化因子,补体系统被激活,软骨降解因子如基质金属蛋白(MMP)和前列腺素E2(PGE2)被释放,导致关节软骨进一步受损。使用抗细胞因子疗法治疗类风湿性关节炎取得了相当大的成功。然而,对于 OA,这些疗法并没有显示出太大的效果,这凸显了 OA 发病机制更加复杂的本质。这需要开发更多新的治疗 OA 的方法,其中可能包括作用于多个靶点的疗法。植物天然产物具有这种特性,可以考虑用于未来的药物开发工作。在此,我们回顾了有关免疫系统不同组成部分在 OA 发病机制中的研究。
Even though osteoarthritis (OA) is mainly considered as a degradative condition of the articular cartilage, there is increasing body of data demonstrating the involvement of all branches of the immune system. Genetic, metabolic or mechanical factors cause an initial injury to the cartilage resulting in release of several cartilage specific auto-antigens, which trigger the activation of immune response. Immune cells including T cells, B cells and macrophages infiltrate the joint tissues, cytokines and chemokines are released from different kind of cells present in the joint, complement system is activated, cartilage degrading factors such as matrix metalloproteins (MMPs) and prostaglanding E2 (PGE2) are released, resulting in further damage to the articular cartilage. There is considerable success in the treatment of rheumatoid arthritis using anti-cytokine therapies. In OA, however, these therapies did not show much effect, highlighting more complex nature of pathogenesis of OA. This needs the development of more novel approaches to treat OA, which may include therapies that act on multiple targets. Plant natural products have this kind of properties and may be considered for future drug development efforts. Here we reviewed the studies implicating different components of the immune system in the pathogenesis of OA.
滑膜巨噬细胞和巨噬细胞产生的细胞因子在驱动聚集蛋白聚糖酶、基质金属蛋白酶和骨关节炎中其他破坏性和炎症反应中的作用。
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