Pristane primed rat T cells enhance TLR3 expression of fibroblast-like synoviocytes via TNF-α initiated p38 MAPK and NF-κB pathways

Wenhua Zhu; Congshan Jiang; Jing Xu; Manman Geng; Xiaoying Wu; Jian Sun; Jie Ma; Rikard Holmdahl; Liesu Meng; Shemin Lu

doi:10.1016/j.clim.2014.11.008

Pristane primed rat T cells enhance TLR3 expression of fibroblast-like synoviocytes via TNF-α initiated p38 MAPK and NF-κB pathways

Wenhua Zhu
, Congshan Jiang
, Jing Xu
, Manman Geng
, Xiaoying Wu
, Jian Sun
, Jie Ma
, Rikard Holmdahl
, Liesu Meng
, Shemin Lu

医学部

Xi'an Jiaotong University
Karolinska Institutet

科研成果: 期刊稿件 › 文章 › 同行评审

21 引用（Scopus）

摘要

Based on pristane-induced arthritis (PIA), we found that T cells mediate TLR3 overexpression in fibroblast-like synoviocytes (FLS). The aim of this study is to determine key factors by which T cells induce TLR3 expression. Rat FLS were co-cultured with pristane primed T cell conditioned medium (PPT medium), and TLR3 expression of FLS was significantly induced. TNF-α, IFN-γ and IL-17 were dominantly expressed in PIA T cells. The overexpression of TLR3 and its related genes in FLS co-cultured with PPT medium could be reduced through blocking TNF-α pathway. CD4⁺ T cells from spleen of PIA rats showed increase of TNF-α secretion. P38 MAPK and NF-κB were activated in FLS by PPT medium, and their inhibitors decreased TLR3 upregulation significantly. Finally, TNF-α induced TLR3 expression was confirmed in human synovial cells.

源语言	英语
页（从-至）	141-153
页数	13
期刊	Clinical Immunology
卷	156
期	2
DOI	https://doi.org/10.1016/j.clim.2014.11.008
出版状态	已出版 - 1 2月 2015

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10.1016/j.clim.2014.11.008

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title = "Pristane primed rat T cells enhance TLR3 expression of fibroblast-like synoviocytes via TNF-α initiated p38 MAPK and NF-κB pathways",

abstract = "Based on pristane-induced arthritis (PIA), we found that T cells mediate TLR3 overexpression in fibroblast-like synoviocytes (FLS). The aim of this study is to determine key factors by which T cells induce TLR3 expression. Rat FLS were co-cultured with pristane primed T cell conditioned medium (PPT medium), and TLR3 expression of FLS was significantly induced. TNF-α, IFN-γ and IL-17 were dominantly expressed in PIA T cells. The overexpression of TLR3 and its related genes in FLS co-cultured with PPT medium could be reduced through blocking TNF-α pathway. CD4+ T cells from spleen of PIA rats showed increase of TNF-α secretion. P38 MAPK and NF-κB were activated in FLS by PPT medium, and their inhibitors decreased TLR3 upregulation significantly. Finally, TNF-α induced TLR3 expression was confirmed in human synovial cells.",

keywords = "Cytokines, Experimental arthritis, Fibroblast-like synoviocyte, T cells, TLR3",

author = "Wenhua Zhu and Congshan Jiang and Jing Xu and Manman Geng and Xiaoying Wu and Jian Sun and Jie Ma and Rikard Holmdahl and Liesu Meng and Shemin Lu",

note = "Publisher Copyright: {\textcopyright} 2014 Elsevier Inc.",

year = "2015",

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doi = "10.1016/j.clim.2014.11.008",

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T1 - Pristane primed rat T cells enhance TLR3 expression of fibroblast-like synoviocytes via TNF-α initiated p38 MAPK and NF-κB pathways

AU - Zhu, Wenhua

AU - Jiang, Congshan

AU - Xu, Jing

AU - Geng, Manman

AU - Wu, Xiaoying

AU - Sun, Jian

AU - Ma, Jie

AU - Holmdahl, Rikard

AU - Meng, Liesu

AU - Lu, Shemin

PY - 2015/2/1

Y1 - 2015/2/1

N2 - Based on pristane-induced arthritis (PIA), we found that T cells mediate TLR3 overexpression in fibroblast-like synoviocytes (FLS). The aim of this study is to determine key factors by which T cells induce TLR3 expression. Rat FLS were co-cultured with pristane primed T cell conditioned medium (PPT medium), and TLR3 expression of FLS was significantly induced. TNF-α, IFN-γ and IL-17 were dominantly expressed in PIA T cells. The overexpression of TLR3 and its related genes in FLS co-cultured with PPT medium could be reduced through blocking TNF-α pathway. CD4+ T cells from spleen of PIA rats showed increase of TNF-α secretion. P38 MAPK and NF-κB were activated in FLS by PPT medium, and their inhibitors decreased TLR3 upregulation significantly. Finally, TNF-α induced TLR3 expression was confirmed in human synovial cells.

AB - Based on pristane-induced arthritis (PIA), we found that T cells mediate TLR3 overexpression in fibroblast-like synoviocytes (FLS). The aim of this study is to determine key factors by which T cells induce TLR3 expression. Rat FLS were co-cultured with pristane primed T cell conditioned medium (PPT medium), and TLR3 expression of FLS was significantly induced. TNF-α, IFN-γ and IL-17 were dominantly expressed in PIA T cells. The overexpression of TLR3 and its related genes in FLS co-cultured with PPT medium could be reduced through blocking TNF-α pathway. CD4+ T cells from spleen of PIA rats showed increase of TNF-α secretion. P38 MAPK and NF-κB were activated in FLS by PPT medium, and their inhibitors decreased TLR3 upregulation significantly. Finally, TNF-α induced TLR3 expression was confirmed in human synovial cells.

KW - Cytokines

KW - Experimental arthritis

KW - Fibroblast-like synoviocyte

KW - T cells

KW - TLR3

UR - https://www.scopus.com/pages/publications/84920929252

U2 - 10.1016/j.clim.2014.11.008

DO - 10.1016/j.clim.2014.11.008

M3 - 文章

C2 - 25533241

AN - SCOPUS:84920929252

SN - 1521-6616

VL - 156

SP - 141

EP - 153

JO - Clinical Immunology

JF - Clinical Immunology

IS - 2

ER -

Pristane primed rat T cells enhance TLR3 expression of fibroblast-like synoviocytes via TNF-α initiated p38 MAPK and NF-κB pathways

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