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Tumor Cell-Intrinsic Factors Underlie Heterogeneity of Immune Cell Infiltration and Response to Immunotherapy. 2018
Jinyang Li, and
Katelyn T Byrne, and
Fangxue Yan, and
Taiji Yamazoe, and
Zeyu Chen, and
Timour Baslan, and
Lee P Richman, and
Jeffrey H Lin, and
Yu H Sun, and
Andrew J Rech, and
David Balli, and
Ceire A Hay, and
Yogev Sela, and
Allyson J Merrell, and
Shannon M Liudahl, and
Naomi Gordon, and
Robert J Norgard, and
Salina Yuan, and
Sixiang Yu, and
Timothy Chao, and
Shuai Ye, and
T S Karin Eisinger-Mathason, and
Robert B Faryabi, and
John W Tobias, and
Scott W Lowe, and
Lisa M Coussens, and
E John Wherry, and
Robert H Vonderheide, and
Ben Z Stanger
Abramson Family Cancer Research Institute, University of Pennsylvania, 3400 Civic Center Blvd., Philadelphia, PA 19104, USA.
The biological and functional heterogeneity between tumors-both across and within cancer types-poses a challenge for immunotherapy. To understand the factors underlying tumor immune heterogeneity and immunotherapy sensitivity, we established a library of congenic tumor cell clones from an autochthonous mouse model of pancreatic adenocarcinoma. These clones generated tumors that recapitulated T cell-inflamed and non-T-cell-inflamed tumor microenvironments upon implantation in immunocompetent mice, with distinct patterns of infiltration by immune cell subsets. Co-injecting tumor cell clones revealed the non-T-cell-inflamed phenotype is dominant and that both quantitative and qualitative features of intratumoral CD8+ T cells determine response to therapy. Transcriptomic and epigenetic analyses revealed tumor-cell-intrinsic production of the chemokine CXCL1 as a determinant of the non-T-cell-inflamed microenvironment, and ablation of CXCL1 promoted T cell infiltration and sensitivity to a combination immunotherapy regimen. Thus, tumor cell-intrinsic factors shape the tumor immune microenvironment and influence the outcome of immunotherapy.
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