期刊
CANCER LETTERS
卷 351, 期 1, 页码 162-171出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2014.05.010
关键词
Mouse; Liver transplantation; Graft; Immune-environment; Allogeneic
类别
资金
- Fundamental Research Funds for the Central Universities [2013FZA7009]
- Foundation for Innovative Research Groups of the National Natural Science Foundation of China [81121002]
- National Natural Science Foundation of China [81372626]
- Natural Science Foundation of Zhejiang province [LQ13H030001, Y2110064]
Liver transplantation is a final therapeutic option for treatment of hepatic malignancies, but local recurrence remains high after surgery. However, the underlying mechanisms of local tumor recurrence are still unknown. We speculated that immunological status of transplanted liver may contribute to the progress of tumor development. CT-26 tumor cells are injected into graft after allogeneic or syngeneic liver transplantation. The growth pattern of tumor and the co-relationship of regulatory T cell and effector T cells in liver graft were observed and investigated at 3d, 6d, 9d and 15d post-transplantation. The Hepatic Replacement Area of tumor in allogeneic grafts was significantly larger than that in syngeneic grafts. The activation of tumor growth in allografts was due to the dysfunction of effector T cells mediated by regulatory T cells in liver graft. Using nude mice model, we further confirmed that regulatory T cells from allograft significantly weaken the function of effector T cells in vivo. Our data has showed that MHC-mismatched mice liver transplantation can promote tumor growth in liver graft. For the first time, we demonstrated that susceptibility to tumor development in liver graft is due to the down-regulation of effector T cells' function mediated by the regulatory T cells. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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