T细胞是GVHD主要效应细胞，胸腺是T细胞重建中枢场所。我们前期研究提出MSC通过TEC途径重塑胸腺、诱导免疫耐受与促进T细胞重建是MSC抑制GVHD而不增加感染和白血病复发的机制之一，但确切机理需深入研究。我们及国内外新近研究发现aGVHD受体存在胸腺MSC和ILC丢失，MSC与ILC均可促进TEC增殖、且两者在组织修复中相互协同。基于以上我们推测MSC-ILC-TEC轴异常是胸腺不能重建移植后正常免疫的原因并提出：MSC通过MSC-ILC-TEC轴重塑受体胸腺结构和改善其功能的假说。为验证该假说，拟在体外、动物模型和aGVHD患者中研究：aGVHD条件下胸腺MSC、ILC和TEC损伤与机理及在GVHD中作用与机理；MSC-ILC-TEC相互作用及对胸腺和T细胞重建影响与机理。通过这些研究揭示MSC-ILC-TEC轴在重塑胸腺中的作用及机理，为构建MSC及ILC防治GVHD提供理论依据。

T cell is the main effector cell of GVHD, and thymus is the central site of T cell reconstruction post-transplantation. Our previous study suggested that MSC remodels thymus via TEC, inducing immune tolerance and promoting T cell reconstitution, and it is one of the mechanisms that MSC inhibits GVHD without increasing infections and leukemia recurrence. But, the exact mechanism needs to be further studied. Some recent studies including our studies have found that aGVHD receptors have a deletion of thymic MSC and ILC. Both MSC and ILC can promote TEC proliferation, and they have synergistic effects in tissue repair. Based on the above, we hypothesize that the abnormality of MSC-ILC-TEC axis is the reason that thymus cannot reconstruct the normal immunity post-transplantation, and MSC remodels thymus tissue structure and improves its function through the MSC-ILC-TEC axis. To validate this hypothesis, we intend to study in vitro, animal models, and the patients with aGVHD: Thymic MSC, ILC and TEC damages and its mechanisms under aGVHD conditions; the roles of thymic MSC, ILC and TEC on the development of GVHD; the effects of the cross-talk between MSC-ILC-TEC on promoting thymic remodeling and T cell reconstitution, and its mechanism. These studies will make known the role and mechanism of MSC-ILC-TEC axis in thymus remodeling, and provide a theoretical basis for MSC and ILC preventing and treating GVHD.