期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 214, 期 12, 页码 3565-3575出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20170356
关键词
-
资金
- National Institutes of Health/National Cancer Institute Cancer Center Support Grant [P30CA008748]
- National Institutes of Health [R37AI034206]
- Ludwig Center at Memorial Sloan Kettering Cancer Center
- Hilton-Ludwig Cancer Prevention Initiative
- Irvington Fellowship of the Cancer Research Institute
- Robert Black Fellowship of the Damon Runyon Cancer Research Foundation [DRG-2143-13]
The involvement of effector T cells and regulatory T (T reg) cells in opposing and promoting solid organ carcinogenesis, respectively, is viewed as a shifting balance between a breach versus establishment of tolerance to tumor or self-antigens. We considered that tumor-associated T cells might promote malignancy via distinct mechanisms used by T cells in nonlymphoid organs to assist in their maintenance upon injury or stress. Recent studies suggest that T reg cells can participate in tissue repair in a manner separable from their immunosuppressive capacity. Using transplantable models of lung tumors in mice, we found that amphiregulin, a member of the epidermal growth factor family, was prominently up-regulated in intratumoral T reg cells. Furthermore, T cell-restricted amphiregulin deficiency resulted in markedly delayed lung tumor progression. This observed deterrence in tumor progression was not associated with detectable changes in T cell immune responsiveness or T reg and effector T cell numbers. These observations suggest a novel nonimmune modality for intratumoral T reg and effector T cells in promoting tumor growth through the production of factors normally involved in tissue repair and maintenance.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据