供体传播性肿瘤（Donor Transmitted Malignancy, DTM）新近成为器官移植的研究热门，其意义在于：如果解决DTM问题，将极大地缓解器官短缺问题，并为肿瘤免疫研究提供新思路。目前国内外缺乏DTM相关的基础研究。我们在前期利用小鼠肝移植DTM模型发现：肝脏免疫微环境中TNFR2阳性的调节性T细胞以及上游Galectin-1是DTM肿瘤逃避受体同种异体免疫反应的机制。因此在本研究中，我们拟进一步研究DTM的生长模式、与受体免疫的相互作用等问题，并通过阻断性抗体、siRNA干扰、可溶性抗体竞争抑制等方法特异性地清除TNFR2 阳性调节性T细胞；阻断Galectin-1；同时通过阻断肿瘤浸润的调节性T细胞特异性的趋化系统CCL22-CCR6等阻止调节性T细胞进入肿瘤灶，从而在不影响移植肝免疫耐受的基础上，达到防治DTM的目的。

Recently, donor transmitted malignancy ( DTM ) is focused due to the shortage of organs and the using of marginal tumor-bearing-donors. Targeting DTM will effectively expand the donor pools, and bring new method for biotherapy of cancer. Previously, we found the tumor specific TNFR2 positive regulatory T cells(Tregs) and Galectin-1 were essential for the growth of DTM in a murine liver transplantation model, by inhibiting the allogeneic response toward the tumor cells. Therefore, we plan to research the growth pattern of DTM and the effects of allogeneic immunity to DTM in liver grafts. Besides,we try to establish a new therapie to reduce the risk of DTM without increasing the risk of graft rejection by specifically deleting TNFR2 positive Tregs,blocking Galectin-1 pathway and specific chemotaxis which Tregs need for inflitrating into tumor sites.