TIGIT/CD226-CD155通路在Helios+FoxP3+Tregs细胞介导的角膜移植免疫耐受中的调控研究

调节性T细胞（Tregs）在角膜移植中发挥重要免疫抑制作用，以往的研究多关注于FoxP3+Tregs细胞的调控。最新研究发现Helios，而不是FoxP3，是活化的Tregs细胞的标记物。TIGIT可以有效区分Helios+FoxP3+Tregs细胞与Helios-FoxP3+Tregs细胞，而TIGIT和CD226与其配体CD155共同调控这一通路的免疫应答。因此，TIGIT/CD226-CD155通路可能实现对Helios+FoxP3+Tregs细胞的功能性调控，从而抑制免疫排斥反应的发生。本课题拟通过体外扩增CD155调控的Helios+FoxP3+Tregs细胞，观察其免疫抑制功能。进一步利用TIGIT或CD226单克隆抗体腹腔注射于受体小鼠，或将调控的细胞过继转移到受体小鼠，观察角膜移植术后植片的存活时间，为防治角膜移植免疫排斥反应提供新的方法。

Regulatory T cells (Tregs) play an important role in immunosuppression in corneal transplantation. Previous studies mostly focused on the regulation of FoxP3+Tregs cells. A recent research has found out that Helios, instead of FoxP3, is a marker for activated Tregs cells. TIGIT can effectively distinguish Helios+FoxP3+Tregs cells from Helios-FoxP3+Tregs cells. Furthermore, TIGIT, CD226 and their ligand CD155 regulate the immune response of this pathway collectively. Therefore, the TIGIT/CD226-CD155 pathway may control the functional regulation of Helios+FoxP3+Tregs cells, thereby inhibiting the occurrence of immune rejection. This research aims to observe the immunosuppressive function of Helios+FoxP3+Tregs cells regulated by CD155 in vitro. And inject TIGIT or CD226 monoclonal antibody into recipient mice by intraperitoneal injection, or adoptive transfer of regulatory cells to recipient mice, to observe the survival time of grafts after corneal transplantation, providing new prevention and treatment for corneal allograft rejection.