免疫学
关节炎
类风湿性关节炎
炎症
免疫系统
酪氨酸激酶
滑膜炎
医学
自身免疫性疾病
癌症研究
炎性关节炎
受体
抗体
内科学
作者
Ziye Wang,Zhen Zhao,Zhichang Li,Liling Xu,Hongchao Li,Honglan Zhu,Gong Chen,Ranran Yao,Wenwen Pei,Rui Liang,Renge Liang,Hua Ye,Shan Jiang,Haitao Niu,Xiaolin Sun,Yin Su
标识
DOI:10.1016/j.clim.2023.109753
摘要
Rheumatoid arthritis (RA) is a systemic autoimmune disorder characterized by synovitis and joint damage, the underlying causes of which remain unclear. Our prior investigations revealed a notable correlation between the expression of Tyro3 Protein Tyrosine Kinase (Tyro3TK) and the progression of RA. To further elucidate the pathogenic role of Tyro3TK in RA, we analyzed the influence of Tyro3TK on pathogenic phenotypes of RA fibroblast like synoviocyte (FLS) in vitro and compared disease severity, joint damages and immunological parameters of K/BxN serum transfer arthritis (STA) in Tyro3TK−/− deficient mice and wild type controls. Our findings underscored the remarkable effectiveness of Tyro3TK blockade, as evidenced by diminished secretion of inflammatory cytokines and matrix metalloproteinases (MMPs), curtailed migration and invasiveness of RAFLS, and attenuated differentiation of pathogenic helper T cell subsets mediated by RAFLS. Correspondingly, our in vivo investigations illuminated the more favorable outcomes in Tyro3TK-deficient mice, characterized by reduced joint pathology, tempered synovial inflammation, and restored immune cell equilibrium. These data suggested that Tyro3TK might contribute to aggravated autoimmune arthritis and immunological pathology and act as a potential therapeutic target for RA.
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