角膜盲是我国第二大致盲性眼病，一般需角膜移植手术复明，然而术后免疫排斥反应是移植失败的最主要原因。最新研究表明对移植物进行识别和攻击的免疫细胞群，如抗原递呈细胞和效应T细胞，主要借助有氧糖酵解途径获得能量从而发挥其免疫功能。本团队前期研究结果：有氧糖酵解代谢相关蛋白葡萄糖转运蛋白GLUT1、乳酸脱氢酶LDHA等在免疫排斥角膜组织中高表达，抑制糖酵解过程可显著延缓角膜移植免疫排斥反应的发生。因此，我们推测：有氧糖酵解途径是抗原递呈细胞以及效应T细胞的发挥其免疫识别和攻击功能的关键能量开关，在角膜移植免疫排斥反应中发挥重要作用。为验证上述假说，我们拟采用小鼠高危角膜移植模型，结合体内外实验，探讨有氧糖酵解途径通过调控抗原递呈细胞和效应T细胞功能参与角膜移植术后免疫排斥反应的机制。通过本研究不仅可以明确有氧糖酵解途径对免疫排斥反应的影响及其机制，还可以为临床防治角膜移植免疫排斥反应提供理论依据。

AS the second largest blind eye diseases, the corneal blindness needs keratoplasty for eyesight restoration. However, immune rejection is the main cause of corneal allograft failure. Emerging evidence indicates that activated antigen-presenting cells (APCs) and effector T cells（Teffs）recognize and attack allografts mainly through aerobic glycolysis. Our previous study have found that the proteins involved in aerobic glycolysis, such as glucose transporter GLUT1 and lactate dehydrogenase LDHA, were highly expressed in rejected corneal allografts. Blockade of glycolysis could significantly prevent corneal allograft rejection. Based on these observations, we hypothesize that aerobic glycolysis, as a key energy switch, plays an important role in the high-risk corneal allograft rejection by regulating APCs and Teffs. To verify this hypothesis, here we will investigate the mechanisms of aerobic glycolysis involved in the high-risk corneal allograft rejection through regulating the functions of APCs and Teffs. Our investigation will not only elucidate the effect and mechanism of anaerobic glycolysis on corneal allograft rejection, but also provide a theoretical basis for clinical prevention and treatment of corneal allograft rejection.