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 intra-vital 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.
Author Info: (1) Department of Pathology, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA. (2) Department of Pathology, The University of Chicago, 5841 Sou
Author Info: (1) Department of Pathology, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA. (2) Department of Pathology, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA. (3) Department of Pathology, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA. (4) Department of Pathology, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA; Department of Medicine, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA. Electronic address: tgajewsk@medicine.bsd.uchicago.edu.
