目前已证实口服抗原能够有效抑制移植排斥反应，为实现移植物长期存活提供了新思路。研究表明：肠黏膜一方面通过分泌免疫负调因子及诱导Treg形成促使免疫耐受状态发生，另一方面，通过控制黏膜通透性抑制外来抗原直接激活肠道免疫系统，共同维持耐受状态，但其机制尚不清楚。我们前期研究初步阐明肠黏膜TCRγδIEL在诱导Treg形成中起重要作用；同时有研究显示该类IEL通过分泌KGF在维持肠黏膜通透性中起关键作用，而KGF能诱导外周血Treg增殖。提示，在肠道，TCR γδ IEL也可通过分泌KGF，一方面促进Treg细胞增殖，增强免疫耐受，另一方面防止肠粘膜屏障破坏，维持耐受状态。本课题拟采用口服抗原小鼠肾移植模型，探讨肠黏膜TCRγδIEL通过分泌KGF诱导Treg形成促进耐受发生以及分泌KGF控制膜通透性、降低免疫激活，进而抑制排斥反应的作用及其机制，为临床应用口服耐受减轻移植排斥反应奠定基础。

It has been confirmed that graft rejection could be inhibited by oral administration of antigen, which provided a new way for long-term survival of the graft. On the one hand, oral tolerance could be induced by the secretion of immune suppression factor and promotion of Treg formation, and on the other hand, the tolerance might be maintained by controlling the membrane permeability, which thus inhibited direct antigen activation of intestinal immune system. But the underlined mechanism is unclear. Our preliminary study showed that the TCR gamma delta IEL played an important role in the induction of Treg formation. It is showed that this kind of IEL played a key role in the maintenance of intestinal mucosal permeability by secreting KGF and KGF could induce the proliferation of Tregs in peripheral blood . These data indicated that in the gut, TCR gamma delta IEL,by secreting KGF, might also promote the proliferation of Tregs and prevent the antigen activation by controlling the mucus permeability ,which might be the important bases for oral tolerance maintenance. The aim of this study is to explore the effect of IEL and secreting KGF on the tolerance induction and the underlining mechanisms in a kidney transplantation model, which could lay the foundation for clinical induction of oral tolerance.