Yang Ying-Li, Li Xiao-Feng, Song Biao, Wu Sha, Wu Yuan-Yuan, Huang Cheng, Li Jun
Inflammation and Immune Mediated Disease Laboratory of Anhui Province, The Key Laboratory of Anti-Inflammatory and Immune Medicines, Ministry of Education, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, 230032, China.
Department of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei, 230032, China.
Rheumatol Ther. 2023 Aug;10(4):793-808. doi: 10.1007/s40744-023-00554-0. Epub 2023 May 25.
Rheumatoid arthritis (RA) is a chronic autoimmune disease of unexplained causes. Its pathological features include synovial tissue hyperplasia, inflammatory cell infiltration in joint cavity fluid, cartilage bone destruction, and joint deformation. C-C motif chemokine ligand 3 (CCL3) belongs to inflammatory cell chemokine. It is highly expressed in inflammatory immune cells. Increasingly, studies have shown that CCL3 can promote the migration of inflammatory factors to synovial tissue, the destruction of bone and joint, angiogenesis, and participate in the pathogenesis of RA. These symptoms indicate that the expression of CCL3 is highly correlated with RA disease. Therefore, this paper reviews the possible mechanism of CCL3 in the pathogenesis of RA, which may provide some new insights for the diagnosis and treatment of RA.
类风湿关节炎(RA)是一种病因不明的慢性自身免疫性疾病。其病理特征包括滑膜组织增生、关节腔液中炎性细胞浸润、软骨骨破坏和关节变形。C-C基序趋化因子配体3(CCL3)属于炎性细胞趋化因子。它在炎性免疫细胞中高表达。越来越多的研究表明,CCL3可促进炎性因子向滑膜组织迁移、骨关节破坏、血管生成,并参与类风湿关节炎的发病机制。这些症状表明CCL3的表达与类风湿关节炎疾病高度相关。因此,本文综述了CCL3在类风湿关节炎发病机制中的可能作用机制,这可能为类风湿关节炎的诊断和治疗提供一些新的见解。