ILCs介导的CD4+T细胞免疫调节在口腔扁平苔藓炎症反应中的作用及机制研究

口腔扁平苔藓（OLP）是一种以T细胞介导的免疫应答为特征的口腔黏膜慢性炎症性疾病。固有淋巴样细胞（ILCs）调控黏膜屏障及免疫炎症应答。本课题以ILCs介导的CD4+T细胞免疫调节为切入点，提出ILCs通过调控抗原提呈，CD4+T细胞的活化、分化、增殖、募集、凋亡，细胞因子分泌，角质形成细胞（KCs）的紧密连接屏障功能和炎症应答，影响OLP的发生发展。拟研究OLP ILCs亚群分类、表型特征及效应功能；OLP ILCs对CD4+T细胞的免疫调节作用及机制；ILCs对 KCs 紧密连接屏障功能和炎症应答的影响；JAK/STAT、mTOR、miRNA调控OLP ILCs免疫功能；OLP细胞因子微环境对ILCs可塑性的影响；ILCs在小鼠口腔黏膜炎症反应中的作用和机制。本项目为丰富OLP的免疫炎症发病机制，寻找基于ILCs的治疗新途径提供了理论基础和实验依据，具有重要科学价值及应用前景。

Oral lichen planus (OLP) is a chronic inflammatory disease of oral mucosa characterized by T cell-mediated immune response. Innate lymphoid cells（ILCs）play important roles in regulating the mucosal barrier and immune inflammatory response. This study takes the immune regulation of CD4+T cells mediated by ILCs as the breakthrough point, and proposes that ILCs can affect the occurrence and development of OLP by regulating antigen presentation, activation, differentiation, proliferation, migration, apoptosis, cytokine secretion of CD4+T cells, and tight junction barrier function and inflammatory response of keratinocytes (KCs). To test this hypothesis, the present study will (1) analyze the classification, phenotypic characteristics and effect function of OLP ILCs subsets; (2) explore the immunomodulatory effect of OLP ILCs on CD4+T and its mechanism; (3) probe the effect of ILCs on KCs tight junction barrier function and inflammatory response (4) seek the mechanisms by which JAK/STAT, mTOR and miRNA regulate the immune function of OLP ILCs; (5) discover the regulation and mechanism of OLP cytokine microenvironment on the plasticity of ILCs; (6) search the role and mechanisms of ILCs in inflammatory response of oral mucosa in mice. This project potentially provides a theoretical basis and experimental basis for enriching the inflammatory immune mechanism of OLP and seeking a new treatment approach based on ILCs, which has important scientific value and promising application prospect.