TL1A increased IL-6 production on fibroblast-like synoviocytes by preferentially activating TNF receptor 2 in rheumatoid arthritis
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- 作者：Zijian Maa ; 1 ; Bing Wanga ; 1 ; Miaomiao Wanga ; b ; Xiaotong Suna ; Yawei Tanga ; Ming Lia ; Fang Lia ; Xia Lia ; Lixia416@163.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：TL1A ; tumor necrosis factor-like protein 1A ; DR3 ; death receptor 3 ; RA ; rheumatoid arthritis ; FLS ; fibroblast-like synoviocytes ; IL ; interleukin ; Th17 ; IL-17-producting helper T cells ; DcR3 ; decoy receptor 3 ; MMPs ; matrix metallo-proteinase ; NF-κB ; nuclear factor κB ; MAPK ; mitogen-activated protein kinase ; TNF ; tumor necrosis factor ; PBMC ; peripheral blood mononuclear cell ; HC ; healthy control ; ELISA ; enzyme-linked immunosorbent assay ; RT-PCR ; reverse transcription polymerase chain reaction ; ESR
- 刊名：Cytokine
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：83
- 期：Complete
- 页码：92-98
- 全文大小：1572 K
文摘
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TL1A was capable of acting on RA FLS to increase the expression of IL-6, which promoted the production of Th17.
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TL1A could influence RA FLS through binding to TNFR2 rather than DR3 on FLS.
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TL1A increased the production of IL-6 by RA FLS possibly via NF-κB and JNK signaling pathway.
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20">TL1A could promote RA FLS to secrete some immune molecules associated with inflammation and autoimmune diseases.