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Cancer Cell. 2017 May 8;31(5):711-723.e4. doi: 10.1016/j.ccell.2017.04.003.

Tumor-Residing Batf3 Dendritic Cells Are Required for Effector T Cell Trafficking and Adoptive T Cell Therapy.

Author information

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; Department of Medicine, The University of Chicago, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637, USA. Electronic address: tgajewsk@medicine.bsd.uchicago.edu.

Abstract

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.

KEYWORDS:

T cell-inflamed tumor microenvironment; adoptive T cell transfer; immune escape; immunotherapy resistance; non-T cell-inflamed tumor microenvironment

PMID:
28486109
PMCID:
PMC5650691
DOI:
10.1016/j.ccell.2017.04.003
[Indexed for MEDLINE]
Free PMC Article

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