IL-36α contributes to enhanced T helper 17 type responses in allergic rhinitis

被引:15
|
作者
Qin, Xiaowei [1 ]
Zhang, Tianhong [1 ]
Wang, Chunrui [1 ]
Li, Huijun [1 ]
Liu, Ming [2 ]
Sun, Yanan [2 ]
机构
[1] Harbin Med Univ, Dept Otolaryngol, Affiliated Hosp 1, Harbin, Peoples R China
[2] Harbin Med Univ, Dept Otolaryngol, Affiliated Hosp 2, Harbin, Peoples R China
基金
中国国家自然科学基金;
关键词
Interleukin-36; alpha; Th17; cells; Allergic rhinitis; CELLS; INFLAMMATION; REGULATORS; ACTIVATION; LIGANDS; AXIS;
D O I
10.1016/j.cyto.2020.154992
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 upregulated significantly compared with controls. The IL-36 alpha promoted the differentiation and function of Th17 cells. The anti-IL-36 alpha 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-36 alpha was involved in the regulation of Th17 responses in allergic rhinitis.
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页数:6
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