经IL-33刺激Ⅱ型固有淋巴细胞(ILC2)可产生Th2型细胞因子。我们已在T细胞缺陷但保留ILC2鼠中诱导出过敏症状，并观察到变应性鼻炎(AR)鼠鼻黏膜有IL-33及其受体ST2表达，说明以ILC2为代表的黏膜固有免疫可参与鼻过敏反应。据报道miR-155可通过RNA-RNA的相互作用调节ILC2的转录子GATA3，从而影响ILC2的增殖和分化，而GATA3是miR-155靶基因，也影响Th2。那么miR-155/GATA3/ILC2以什么机制参与AR炎症过程，以及miR-155能否作为AR靶点，将是本研究关注重点。通过单细胞RNA测序(scRNA-seq)已发现AR鼻黏膜细胞种类和数量已变化，我们提出“鼻黏膜细胞紊乱”的概念。运用scRNA-seq了解AR鼠鼻黏膜细胞病理状态，观察miR-155敲除鼠AR鼻黏膜能否恢复正常和ILC2变化，阐明miR-155调控ILC2的机制。

Type 2 innate lymphoid cells (ILC2), stimulated by IL-33, can produce Th2 cytokines. We had induced allergic symptoms in mice with T-cell development defect but ILC2 retention, and observed a large amount of IL-33 and its receptor ST2 expression in the nasal mucosa, suggesting that mucosal innate immunity represented by ILC2 may be involved in the process of nasal allergic reaction. It has been reported that miR-155 can regulate GATA3, the transcription factor of ILC2, through RNA-RNA interaction, thus affecting the proliferation and differentiation of ILC2. Moreover, GATA3, affected on Th2, is also a target gene of miR-155. The important concern of our study is the mechanism of miR-155/GATA3/ILC2 on inflammatory process of AR and the identification of that miR-155 can be used as a target for AR.The single-cell RNA sequencing (ScRNA-Seq) technology has recently found that the type and number of nasal mucosal cells in AR patients have undergone great changes, and on this basis, we proposed the conception "nasal mucosal cells disorder". In this study, we intend to use this technique to identify whether the AR mice with the intervention or the knockout of miR-155 can restore the nasal mucosal status of normal mice.This study will clarify the disorder of nasal mucosal cells in AR pathological state through ScRNA-Seq technology. We also observe the changes of ILC2 cells in the nasal mucosa of AR mice and detect the specific mechanism of miR-155 regulating ILC2.