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IL-36α contributes to enhanced T helper 17 type responses in allergic rhinitis
Cytokine ( IF 3.7 ) Pub Date : 2020-04-01 , DOI: 10.1016/j.cyto.2020.154992
Xiaowei Qin 1 , Tianhong Zhang 1 , Chunrui Wang 1 , Huijun Li 1 , Ming Liu 2 , Yanan Sun 2
Affiliation  

BACKGROUND T helper 17 (Th17) cell subsets, belongs to CD4+ T cell lineage, are proved to be closely related to pathophysiology of AR recently. The interleukin-36 (IL-36) had been reported to promote the up-regulation of Th17 cytokines in psoriasis. We investigated the regulation of Th17 inflammation by IL-36 family cytokines in allergic rhinitis (AR). METHODS Twenty-one patients with AR and 20 healthy controls were enrolled. The expression of serum protein and mRNA of IL-36 family cytokines between AR and control group were detected and compared. Human peripheral blood mononuclear cells were purified and stimulated by IL-36 cytokines. The transcription factor and production of Th17 cytokines by Th17 cells were evaluated. Mouse model with AR was established to confirm the in vitro results. RESULTS The serum expression of IL-36 cytokines and Th17 cytokines (IL-17 and IL-23) of AR patients were up-regulated significantly compared with controls. The IL-36α promoted the differentiation and function of Th17 cells. The anti-IL-36α treatment could alleviate the Th17 response in AR mice, presented with alleviated symptoms, decreased infiltration of Th17 cells and down-regulated Th17 cytokines expression. CONCLUSIONS IL-36α was involved in the regulation of Th17 responses in allergic rhinitis.

中文翻译:

IL-36α 有助于增强过敏性鼻炎中的 T 辅助 17 型反应

背景T辅助17(Th17)细胞亚群属于CD4+ T细胞谱系,近来被证实与AR的病理生理学密切相关。据报道,白细胞介素 36 (IL-36) 可促进银屑病中 Th17 细胞因子的上调。我们研究了过敏性鼻炎 (AR) 中 IL-36 家族细胞因子对 Th17 炎症的调节。方法 招募了 21 名 AR 患者和 20 名健康对照者。检测并比较AR组与对照组血清蛋白及IL-36家族细胞因子mRNA的表达情况。人外周血单个核细胞被 IL-36 细胞因子纯化和刺激。评估了 Th17 细胞的转录因子和 Th17 细胞因子的产生。建立AR小鼠模型以确认体外结果。结果AR患者血清IL-36细胞因子和Th17细胞因子(IL-17和IL-23)的表达较对照组显着上调。IL-36α 促进 Th17 细胞的分化和功能。抗IL-36α治疗可以减轻AR小鼠的Th17反应,症状减轻,Th17细胞浸润减少,Th17细胞因子表达下调。结论 IL-36α 参与了过敏性鼻炎 Th17 反应的调节。
更新日期:2020-04-01
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