IL-36α 有助于增强变应性鼻炎中的辅助性 T 细胞 17 型应答。
IL-36α contributes to enhanced T helper 17 type responses in allergic rhinitis.
机构信息
Department of Otolaryngology, First Affiliated Hospital to Harbin Medical University, Harbin, China.
Department of Otolaryngology, Second Affiliated Hospital to Harbin Medical University, Harbin, China.
出版信息
Cytokine. 2020 Apr;128:154992. doi: 10.1016/j.cyto.2020.154992. Epub 2020 Jan 23.
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.
背景
辅助性 T 细胞 17（Th17）细胞亚群属于 CD4+T 细胞谱系，最近被证明与变应性鼻炎（AR）的病理生理学密切相关。白细胞介素-36（IL-36）已被报道可促进银屑病中 Th17 细胞因子的上调。我们研究了 IL-36 家族细胞因子在变应性鼻炎（AR）中对 Th17 炎症的调节作用。
方法
纳入 21 例 AR 患者和 20 名健康对照者。检测并比较 AR 组和对照组血清中 IL-36 家族细胞因子的蛋白和 mRNA 表达。纯化人外周血单个核细胞，用 IL-36 细胞因子刺激。评估 Th17 细胞的转录因子和 Th17 细胞因子（IL-17 和 IL-23）的产生。建立 AR 小鼠模型以验证体外结果。
结果
与对照组相比，AR 患者的血清 IL-36 细胞因子和 Th17 细胞因子（IL-17 和 IL-23）表达显著上调。IL-36α 促进了 Th17 细胞的分化和功能。抗-IL-36α 治疗可减轻 AR 小鼠的 Th17 反应，表现为症状减轻、Th17 细胞浸润减少和 Th17 细胞因子表达下调。
结论
IL-36α 参与了变应性鼻炎中 Th17 反应的调节。
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