免疫排斥反应是角膜移植手术失败的最主要原因。间充质干细胞（mesenchymal stem cells，MSCs）具有免疫抑制功能，它在其它组织器官移植排斥方面作用的研究已经开展。白介素-10（interleukin-10，IL-10）具有免疫抑制活性，能够增强机体免疫耐受。慢病毒介导IL-10基因转染MSCs治疗角膜移植排斥反应研究尚未见报道。本研究采用大鼠异体角膜移植排斥模型，观察IL-10基因修饰后的MSCs对角膜移植排斥反应的影响，并通过T细胞增殖实验来检测实验中各组大鼠免疫应答水平，检测因子分泌水平以及CD4+CD25+Foxp3+调节性T细胞的变化，观察其在异体角膜移植大鼠的免疫调节作用，为其在未来临床应用提供基础实验参考依据，进一步明确其免疫调节的关键机理，为角膜移植排斥反应机制的深入研究提供基础，为基因联合细胞治疗角膜移植排斥提供思路和可能。

Although corneal allografts enjoy a remarkable degree of immune privilege, immune rejection remains the leading cause of keratoplasty failure. Mesenchymal stem cells (MSCs) have been proved to have immunosuppressive properties and have been successfully used as cellular therapy in organ transplantation. Immunosuppression activity of Interleukin 10 (IL-10) can enhance the body's immune tolerance. IL-10 has close relationship with cells, cytokine and other immune regulatory factors in the organ transplant rejection. Herein we investigated the immunomodulatory effects of lentivirus-mediated IL-10 gene transfected MSCs on rat corneal allograft rejection model. Recipient corneas were examined following transplant, and rejection was defined according to Larkin. T cell proliferation tests by BrdU to measure the direct suppressive effect. Using ELISA kit to measure the concentrations of cytokine productions related to T helper cells, such as IL-2, IL-4, IL-10, IFN-γ and IL-17. The ratio and expression of CD4+CD25+Foxp3+Tregs, which closely related to Anterior Chamber-Associated Immune Deviation (ACAID), are determined and analyzed by flow cytometry and PCR, respectively..In the present study, we investigated the effect of MSCs on corneal allograft rejection across the full MHC barrier and the therapeutic efficacy of MSCs. We also studied the effects of MSCs on T cell proliferation, on the Th1/Th2 cytokine profiles of T cells, and on the Treg population. We observed that MSCs could inhibit corneal allograft rejection and prolong corneal allograft survival on rat model. This effect might be due to an inhibition of the pro-inflammatory Th1 response and to upregulation of Tregs. These data support the potential use of MSCs as a treatment for corneal allograft rejection. We also gave systemic treat with MSCs alone or MSCs combined with different doses of Cyclosporin A (CsA) in penetrating keratoplasty. Postoperative MSCs injection reduced Th1 pro-inflammatory cytokines and elevated IL-4 cytokine secretion from T lymphocytes derived from cornea-transplanted rats. Tregs were upregulated by MSCs treatment. When 2 mg/kg CsA was given together with MSCs, graft survival was significantly prolonged. In addition, subconjunctival injections of MSCs also prolonged the survival time of cornea allograft, and the MSCs of injected upregulated the expression of IL-10 in the local cornea. Nevertheless, the mechanism of MSCs immunosuppressive properties is not clear, the role of local application is less than the systemic, and CsA's therapeutic dosages are limited by the potentially life-threaten complications associated with immune suppression system and by drug toxicity. Thus, less toxic and more efficient methods of immunomodulation are needed to reduce corneal allograft rejection.