期刊
CANCER CELL
卷 31, 期 5, 页码 711-+出版社
CELL PRESS
DOI: 10.1016/j.ccell.2017.04.003
关键词
-
资金
- Team Science Award from the Melanoma Research Foundation
- Irvington Postdoctoral fellowship by the Cancer Research Institute
- NCI [K99CA204595]
Effector T cells have the capability of recognizing and killing cancer cells. However, whether tumors can become immune resistant through exclusion of effector T cells from the tumor microenvironment is not known. By using a tumor model resembling non-T cell-inflamed human tumors, we assessed whether adoptive T cell transfer might overcome failed spontaneous priming. Flow cytometric assays combined with intravital imaging indicated failed trafficking of effector T cells into tumors. Mechanistically, this was due to the absence of CXCL9/10, which we found to be produced by CD103(+) dendritic cells (DCs) in T cell-inflamed tumors. Our data indicate that lack of CD103(+) DCs within the tumor microenvironment dominantly resists the effector phase of an anti-tumor T cell response, contributing to immune escape.
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