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HMGB1-induced ILC2s activate dendritic cells by producing IL-9 in asthmatic mouse model.
Cellular Immunology ( IF 3.7 ) Pub Date : 2020-03-06 , DOI: 10.1016/j.cellimm.2020.104085
Jie Wan 1 , Lan Huang 1 , Xiaoyun Ji 1 , Shun Yao 2 , Mohamed Hamed Abdelaziz 1 , Wei Cai 1 , Huixuan Wang 1 , Jianjun Cheng 1 , Kesavan Dineshkumar 1 , Vasudevan Aparna 1 , Zhaoliang Su 3 , Shengjun Wang 4 , Huaxi Xu 1
Affiliation  

Asthma is a disease of the respiratory system that is commonly considered a T-helper 2 (Th2) cell-associated inflammatory disease. Group 2 innate lymphoid cells (ILC2s) promote the inflammatory responses in asthma by secreting type 2 cytokines. Interleukin (IL)-9 also serves as a promoting factor in asthma and it is well known that ILC2s have an autocrine effect of IL-9 to sustain their survival and proliferation. However, the specific role of ILC2-derived IL-9 in asthma remains unclear. HMGB1 (High-Mobility Group Box-1) is a nuclear protein, and Previous studies have shown that HMGB1 can regulate the differentiation of T-helper cells and participate in the development of asthma. But whether HMGB1 can regulate the innate lymphocytes in the pathological process of asthma is unknown. In this study we have shown increased presence of HMGB1 protein in the lung of mice with asthma, which was associated with increased secretion of IL-9 by ILC2s. This led to the activation of dendritic cells (DCs) that can accelerate the differentiation of Th2 cells and worsen the severity of asthma. Taken together, our study provides a complementary understanding of the asthma development and highlights a novel inflammatory pathway in the pathogenesis of asthma.

中文翻译:

HMGB1诱导的ILC2通过在哮喘小鼠模型中产生IL-9激活树突状细胞。

哮喘是呼吸系统疾病,通常被认为是T-helper 2(Th2)细胞相关的炎性疾病。第2组先天性淋巴样细胞(ILC2)通过分泌2型细胞因子促进哮喘中的炎症反应。白介素(IL)-9也是哮喘的促进因子,众所周知,ILC2具有IL-9的自分泌作用,以维持其生存和增殖。但是,仍不清楚ILC2衍生的IL-9在哮喘中的具体作用。HMGB1(高迁移率族Box-1)是一种核蛋白,以前的研究表明HMGB1可以调节T辅助细胞的分化并参与哮喘的发展。但是HMGB1在哮喘的病理过程中是否可以调节先天淋巴细胞。在这项研究中,我们显示了哮喘小鼠肺中HMGB1蛋白的存在增加,这与ILC2s分泌的IL-9增加有关。这导致树突状细胞(DC)的激活,可加速Th2细胞的分化并加剧哮喘的严重程度。两者合计,我们的研究提供了对哮喘发展的补充理解,并突出了哮喘发病机理中的新型炎症途径。
更新日期:2020-03-06
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