IL-29 enhances Toll-like receptor-mediated IL-6 and IL-8 production by the synovial fibroblasts from rheumatoid arthritis patients.
IL-29 enhances Toll-like receptor-mediated IL-6 and IL-8 production by the synovial fibroblasts from rheumatoid arthritis patients.
复制标题
IL-29 增强类风湿关节炎患者滑膜成纤维细胞 Toll 样受体介导的 IL-6 和 IL-8 的产生。
DOI：
10.1186/ar4357
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发表时间：
2013-10-29
影响因子：
4.9
通讯作者：
Wang F
中科院分区：
文献类型：
--
作者：
Xu L;Feng X;Tan W;Gu W;Guo D;Zhang M;Wang F
We previously reported that IL-29, a newly described member of interferon (IFN) family, was overexpressed in blood and synovium of rheumatoid arthritis (RA) patients and triggered proinflammatory cytokine IL-6 and IL-8 mRNA expression in RA synovial fibroblasts (RA-FLS). This suggests that IL-29 has an important role in synovial inflammation. Toll-like receptors (TLRs) also activate RA-FLS to produce inflammatory mediators including tumor necrosis factor α (TNF-α) and IL-1β in RA-FLS. Since the TLR family plays an early role in the innate immune response and the subsequent induction of the adaptive immune response, we hypothesize that IL-29 interacts with TLRs in RA inflammation. This study aimed to investigate the effect of IL-29 on TLR-mediated proinflammatory cytokine production in RA-FLS. The mRNA level of IL-29 receptors (IL-28Rα and IL-10R2) in RA-FLS was determined by semi-quantitative RT- PCR. IL-6 and IL-8 mRNA expressions in RA-FLS were evaluated by real-time PCR after pre-incubation with IL-29 and subsequent stimulation with peptidoglycan (PGN, TLR2 ligand), or polycytidylic acid (poly(I:C), TLR3 ligand), or lipopolysaccharide (LPS, TLR4 ligand) . The production of TLR2, 3, and 4 in RA-FLS after IL-29 stimulation was also assessed by real-time PCR and flow cytometry. IL-29 mRNA and protein expression in RA-FLS after stimulation with PGN, poly(I:C), or LPS were measured by real-time PCR and enzyme-linked immunosorbent assay (ELISA), respectively. The IL-29 receptor complex (IL-28Rα and IL-10R2) was identified in RA-FLS. IL-29 enhanced TLR-mediated IL-6 and IL-8 expression in RA-FLS. IL-29 upregulated expression of TLR2, 3 and 4 in RA-FLS. Exposure to PGN, poly(I:C) or LPS triggered IL-29 production by RA-FLS. We show for the first time that IL-29 enhances TLR-induced proinflammatory cytokine production in RA-FLS via upregulation of TLRs.
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影响因子：
12.4
作者：
He, S.;Li, T.;Yang, P.
通讯作者：
Yang, P.
影响因子：
3.6
作者：
Makela, Sanna M.;Osterlund, Pamela;Julkunen, Ilkka
通讯作者：
Julkunen, Ilkka
影响因子：
4.4
作者：
Ank, Nina;Iversen, Marie B.;Paludan, Soren R.
通讯作者：
Paludan, Soren R.
影响因子：
--
作者：
Brentano, F;Schorr, O;Kyburz, D
通讯作者：
Kyburz, D
影响因子：
4.4
作者：
Jung, Young Ok;Cho, Mi-La;Kim, Ho-Youn
通讯作者：
Kim, Ho-Youn