ArticleCell2021
CXCR6 positions cytotoxic T cells to receive critical survival signals in the tumor microenvironment.
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Article in Cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 337 papers.
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337citing papers in PubMed
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337 citing papers in PubMed, 441 citations in OpenAlex.
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277 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 8 institutions in 3 countries.
Mauro Di PilatoCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA; Department of Immunology, The University of Texas MD Anderson Cancer Center, Houston, TX 77054, USA. Electronic address: mdi@mdanderson.org.
Raphael Kfuri-RubensCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Division of Clinical Pharmacology, Department of Medicine IV, Klinikum der Universität München, Munich, Germany.
Jasper N PruessmannCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA.
Aleksandra J OzgaCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA.
Marius MessemakerCenter for Systems Biology, Massachusetts General Hospital, Boston, MA 02115, USA.
Bruno L CadilhaDivision of Clinical Pharmacology, Department of Medicine IV, Klinikum der Universität München, Munich, Germany.
Ramya SivakumarDepartment of Immunology, University of Washington, Seattle, WA 98109, USA.
Chiara CianciarusoHarvard Medical School, Boston, MA 02115, USA; Center for Systems Biology, Massachusetts General Hospital, Boston, MA 02115, USA.
Ross D WarnerCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA.
Francesco MarangoniCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA.
Esteban CarrizosaCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA.
Stefanie LeschDivision of Clinical Pharmacology, Department of Medicine IV, Klinikum der Universität München, Munich, Germany.
James BillingsleyHarvard Chan Bioinformatics Core, Department of Biostatistics, Harvard School of Public Health, Boston, MA 21205, USA.
Daniel Perez-RamosDepartment of Molecular Microbiology and Immunology and Malaria Research Institute, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Fidel ZavalaDepartment of Molecular Microbiology and Immunology and Malaria Research Institute, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Esther RheinbayCenter for Cancer Research, Massachusetts General Hospital, Boston, MA 02129, USA.
Andrew D LusterCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA.
Michael Y GernerDepartment of Immunology, University of Washington, Seattle, WA 98109, USA.
Sebastian KoboldDivision of Clinical Pharmacology, Department of Medicine IV, Klinikum der Universität München, Munich, Germany; German Center for Translational Cancer Research (DKTK), partner site, Munich, Germany.
Mikael J PittetHarvard Medical School, Boston, MA 02115, USA; Center for Systems Biology, Massachusetts General Hospital, Boston, MA 02115, USA; Department of Pathology and Immunology, University of Geneva, Department of Oncology, Geneva University Hospitals, Geneva, Switzerland; Ludwig Institute for Cancer Research, Lausanne Branch, Lausanne, Switzerland.
Thorsten R MempelCenter for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, MA 02129, USA; Harvard Medical School, Boston, MA 02115, USA; Center for Systems Biology, Massachusetts General Hospital, Boston, MA 02115, USA. Electronic address: tmempel@mgh.harvard.edu.
Harvard University · USCenter for Systems Biology · USLMU Klinikum · DEMassachusetts General Hospital · USJohns Hopkins University · USUniversity of Washington · USCenter for Cancer Research · USThe University of Texas MD Anderson Cancer Center · US
Funding
Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3MStrategies to Overcome Immune Resistance in Head and Neck CancersP01CA240239 · NCI · YALE UNIVERSITY · PI PAI, SARA ISABEL · 2019 to 2023
$8.4MCellular mechanisms by which exhausted T cell responses are restoredR01AI123349 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI Thorsten Roman Mempel · 2017 to 2026
$4.5MIn vivo behavior of monocytes in resting and inflammatory conditionsR01AI084880 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI PITTET, MIKAEL · 2011 to 2020
$4.4MThe Roles of Lymphoid Tissue Microenvironments in Guiding the Immune ResponseR01AI134713 · NIAID · UNIVERSITY OF WASHINGTON · PI Michael Gerner · 2018 to 2026
$4.4MSingle Cell Genome-Wide Myeloid Response Profiling in ImmunotherapyR01CA218579 · NCI · HARVARD MEDICAL SCHOOL · PI KLEIN, ALLON MOSHE, PITTET, MIKAEL · 2018 to 2022
$2.7MThe CXCR3 Chemokine System in Cancer ImmunotherapyR01CA204028 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LUSTER, ANDREW D · 2017 to 2021
$1.9MImaging tumor associated macrophage (TAM) functionR01CA206890 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI PITTET, MIKAEL, WEISSLEDER, MD, PHD, RALPH · 2017 to 2021
$1.9MNovel approaches to study the intersection of cellular heterogeneity and tissue microanatomyR21AI142667 · NIAID · UNIVERSITY OF WASHINGTON · PI GERNER, MICHAEL · 2019 to 2020
$485kNCI NIH HHS P01 CA240239NCI NIH HHS R01 CA204028NCI NIH HHS R01 CA206890NCI NIH HHS R01 CA218579NIAID NIH HHS R01 AI084880NIAID NIH HHS R01 AI123349NIAID NIH HHS R01 AI134713NIAID NIH HHS R21 AI142667NIDDK NIH HHS P30 DK043351
Abstract
Cytotoxic T lymphocyte (CTL) responses against tumors are maintained by stem-like memory cells that self-renew but also give rise to effector-like cells. The latter gradually lose their anti-tumor activity and acquire an epigenetically fixed, hypofunctional state, leading to tumor tolerance. Here, we show that the conversion of stem-like into effector-like CTLs involves a major chemotactic reprogramming that includes the upregulation of chemokine receptor CXCR6. This receptor positions effector-like CTLs in a discrete perivascular niche of the tumor stroma that is densely occupied by CCR7
Indexed as
Tumor MicroenvironmentAnimalsB7-H1 AntigenCell CommunicationCell MovementCell ProliferationCell SurvivalChemokine CXCL16Dendritic CellsInterleukin-12Interleukin-15LigandsLymph NodesMelanomaMiceMice, Inbred C57BLB7-H1 AntigenChemokine CXCL16Interleukin-12Interleukin-15LigandsReceptors, CXCR6CCR7(+) dendritic cellsCTLCXCL16CXCR6IL-15multiphoton intravital microscopyscRNA-seqTCF-1TCGAtumor microenvironment
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