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Toll-Like Receptors Expressed by Synovial Fibroblasts Perpetuate Th1 and Th17 Cell Responses in Rheumatoid Arthritis
Hu, Fanlei; Li, Yingni; Zheng, Li; Shi, Lianjie; Liu, Hongjiang; Zhang, Xuewu; Zhu, Huaqun; Tang, Sumei; Zhu, Lei; Xu, Liling; Yang, Yuqin; Li, Zhanguo
刊名PLOS ONE
2014-06-17
DOI10.1371/journal.pone.0100266
9期:6
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]TISSUE ; SYNOVIOCYTES ; BLOCKADE ; DISEASES ; HYPOXIA ; ALPHA ; FLUID ; VIVO ; DNA
英文摘要

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial fibroblast hyperplasia and bone and cartilage erosion. Synovial fibroblast- and T cell-mediated inflammation plays crucial roles in the pathogenesis of RA. However how this inflammation is initiated, propagated, and maintained remains controversial. Here, we systemically examined the contribution of toll-like receptors (TLRs) to the inflammatory mediator production as well as Th1 and Th17 cell hyperactivity in RA. Our results show that rheumatoid arthritis synovial fibroblasts (RASF) express a series of TLRs, including TLR2, TLR3, TLR4, and TLR9, with the predominant expression of TLR3. Moreover, the expression levels of these TLRs were higher than those in osteoarthritis synovial fibroblasts (OASF). Ligation of TLR3, as well as TLR2 and TLR4, resulted in vigorous production of inflammatory cytokines, matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF) in RASF, with activation of the NF-kappa B, MAPK, and IRF3 pathways. More important, activation of these TLRs expressed by RASF exacerbated inflammatory Th1 and Th17 cell expansion both in cell-cell contact-dependent and inflammatory cytokine-dependent manners, which induced more IFN-gamma and IL-17 accumulation. Targeting TLRs may modulate the inflammation in RA and provide new therapeutic strategies for overcoming this persistent disease.

语种英语
WOS记录号WOS:000338503400099
项目编号81302554 ; 81030057 ; 2010CB529100 ; RDB2012-04 ; RDB2013-04
资助机构Natural Science Foundation of China ; 973 program of China ; Peking University People&prime ; s Hospital
引用统计
被引频次:21[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62084
专题北京大学第二临床医学院
北京大学第二临床医学院_风湿免疫科
作者单位Peking Univ, Peoples Hosp, Dept Rheumatol & Immunol, Beijing 100871, Peoples R China
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GB/T 7714
Hu, Fanlei,Li, Yingni,Zheng, Li,et al. Toll-Like Receptors Expressed by Synovial Fibroblasts Perpetuate Th1 and Th17 Cell Responses in Rheumatoid Arthritis[J]. PLOS ONE,2014,9(6).
APA Hu, Fanlei.,Li, Yingni.,Zheng, Li.,Shi, Lianjie.,Liu, Hongjiang.,...&Li, Zhanguo.(2014).Toll-Like Receptors Expressed by Synovial Fibroblasts Perpetuate Th1 and Th17 Cell Responses in Rheumatoid Arthritis.PLOS ONE,9(6).
MLA Hu, Fanlei,et al."Toll-Like Receptors Expressed by Synovial Fibroblasts Perpetuate Th1 and Th17 Cell Responses in Rheumatoid Arthritis".PLOS ONE 9.6(2014).
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