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首页> 外文期刊>Cytokine >TWEAK promotes the production of Interleukin-17 in rheumatoid arthritis
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TWEAK promotes the production of Interleukin-17 in rheumatoid arthritis

机译：TWEAK促进类风湿关节炎中白介素17的产生

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摘要

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is an inflammatory cytokine that modulates several biological responses by inducing chemokines and proinflammatory cytokines. We hypothesized that TWEAK could promote secretion of IL-17, an amplifier of inflammatory arthritis. To test this, we investigated the capacity of TWEAK to induce IL-17 production in T cells via the fibroblast growth factor-inducible gene 14 (Fn14, also known as TWEAK receptor) signal pathway in rheumatoid arthritis (RA). Fn14 and IL-17 were highly expressed in arthritic tissues of collagen-induced arthritis (CIA) mice. TWEAK induced production of IL-17 alone and synergistically with lipopolysaccharide. In na?ve murine T cells, TWEAK promoted Th17 differentiation. The expression of Fn14 was predominant in Th17 cells. TWEAK and IL-17 concentrations were significantly higher in synovial fluid and serum in RA patients than OA patients. In addition, we identified CD4 +IL-17 +Fn14 + cells in synovium from RA patients. TWEAK promoted IL-17 production synergistically with IL-23 or IL-21 and blockade of Fn14 with Fn14-Fc suppressed Th17 differentiation. Conversely, this treatment enhanced Treg differentiation. These results suggest that TWEAK induces IL-17 production and may be a therapeutic target in the treatment of RA.
机译：肿瘤坏死因子（TNF）样的凋亡弱诱导剂（TWEAK）是一种炎症细胞因子，可通过诱导趋化因子和促炎细胞因子来调节多种生物学反应。我们假设TWEAK可以促进炎症性关节炎IL-17的分泌。为了测试这一点，我们研究了风湿性关节炎（RA）中TWEAK通过成纤维细胞生长因子诱导基因14（Fn14，也称为TWEAK受体）信号途径诱导T细胞中IL-17产生的能力。 Fn14和IL-17在胶原诱导的关节炎（CIA）小鼠的关节炎组织中高表达。 TWEAK诱导单独产生IL-17，并与脂多糖协同产生。在幼鼠T细胞中，TWEAK促进Th17分化。 Fn14的表达在Th17细胞中占主导。 RA患者滑液和血清中TWEAK和IL-17的浓度显着高于OA患者。此外，我们从RA患者的滑膜中鉴定出CD4 + IL-17 + Fn14 +细胞。 TWEAK与IL-23或IL-21协同促进了IL-17的产生，而用Fn14-Fc阻断Fn14抑制了Th17分化。相反，这种治疗增强了Treg的分化。这些结果表明，TWEAK诱导IL-17产生，并且可能是RA治疗中的治疗靶标。

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