分泌白介素-17的固有淋巴细胞在哮喘小鼠免疫炎症反应中的作用研究

The imbalance of immunocyte regulation was regarded as one of the important pathogenesis of bronchial asthma. Lymphocyte was considered as the key immunocyte. Abnormal Th17 immunity, which our previous study has found, took part in the pathogenesis of asthma. Th17 mainly produced IL-17, which induce target cells to secrete proinflammatory cytokines to participate in the pathogenesis of asthma. Whereas, Th17 pathway was incompletely explain the early IL-17-midiated immune responses. Besides Th17, new-found IL-17-producing ILC ( ILC)-17 was involved in IL-17-midiated immune inflammatory responses and participated in many immune and inflammatory diseases. However, asthma is an immune and inflammatory disease which involved innate immune and adaptive immune. It is hypothesized that ILC17 were also involved in the pathogenesis of asthma. ILC17 was the early source of IL-17 and could acquire, process and present antigens, migrated to inflammation location, participated directly and then induced and regulated Th17 adaptive immune which all involved in the pathogenesis of asthma. For this purpose, we use wild type BALB/c mice to establish asthmatic model, to investigate the distribution, the ability to acquire, process and present antigens, secretion of ILC17 and effect of ILC17 to Th17 adaptive immune. Our findings may provide a new theoretical basis for the pathogenesis of asthma.

免疫细胞调节失衡是支气管哮喘的重要发病机制之一，其中淋巴细胞是关键免疫细胞。我们前期研究发现异常Th17免疫参与哮喘发病，Th17主要通过分泌IL-17参与哮喘的发病。然而，Th17细胞通路不能全部解释IL-17调节的免疫反应。除Th17外，新发现的分泌IL-17为主的固有淋巴细胞（ILC）-17也是IL-17调节免疫炎症反应的重要组成部分，并参与多种免疫炎症疾病发生。哮喘是由固有免疫和特异性免疫共同参与的一种免疫性疾病，故我们假设ILC17也参与哮喘的发病，其产生于免疫反应早期，摄取呈递抗原，迁移至炎症局部，直接参与以及诱导调节Th17免疫反应共同参与哮喘发生。为此，建立BALB/c哮喘小鼠模型，观察哮喘小鼠不同免疫时期不同组织器官ILC17的分布特点、摄取呈递抗原、迁移等免疫功能以及对Th17特异性免疫的影响，多水平探讨其相关机制，为哮喘发病机制的研究提供新的理论依据。

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