T cell-derived interleukin-22 drives the expression of CD155 by cancer cells to suppress NK cell function and promote metastasis.

Autor:	Briukhovetska D; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Suarez-Gosalvez J; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Voigt C; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Markota A; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Giannou AD; Section of Molecular Immunology and Gastroenterology, I. Department of Medicine, and Hamburg Center for Translational Immunology (HCTI), University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany; Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany., Schübel M; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Jobst J; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Zhang T; Section of Molecular Immunology and Gastroenterology, I. Department of Medicine, and Hamburg Center for Translational Immunology (HCTI), University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany., Dörr J; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Märkl F; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Majed L; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Müller PJ; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., May P; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Gottschlich A; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Tokarew N; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Lücke J; Section of Molecular Immunology and Gastroenterology, I. Department of Medicine, and Hamburg Center for Translational Immunology (HCTI), University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany; Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany., Oner A; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Schwerdtfeger M; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Andreu-Sanz D; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Grünmeier R; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Seifert M; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Michaelides S; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Hristov M; Institute for Cardiovascular Prevention (IPEK), University Hospital, Klinikum der Universität München, Munich, Germany., König LM; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Cadilha BL; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany., Mikhaylov O; TwentyBN, 10245 Berlin, Germany., Anders HJ; Division of Nephrology, Department of Medicine IV, Klinikum der Universität München, 80337 Munich, Germany., Rothenfusser S; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany; Einheit für Klinische Pharmakologie (EKLiP), Helmholtz Zentrum München, German Research Center for Environmental Health (HMGU), 85764 Neuherberg, Germany., Flavell RA; Department of Immunobiology, School of Medicine, Yale University, New Haven, CT 06520, USA; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA., Cerezo-Wallis D; Melanoma Laboratory, Molecular Oncology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain., Tejedo C; Melanoma Laboratory, Molecular Oncology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain., Soengas MS; Melanoma Laboratory, Molecular Oncology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain., Bald T; Institute of Experimental Oncology, Medical Faculty, University Hospital Bonn, University of Bonn, 53127 Bonn, Germany., Huber S; Section of Molecular Immunology and Gastroenterology, I. Department of Medicine, and Hamburg Center for Translational Immunology (HCTI), University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany., Endres S; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany; Einheit für Klinische Pharmakologie (EKLiP), Helmholtz Zentrum München, German Research Center for Environmental Health (HMGU), 85764 Neuherberg, Germany; Center for Translational Cancer Research (DKTK), Partner Site Munich, 80336 Munich, Germany., Kobold S; Division of Clinical Pharmacology, Klinikum der Universität München, 80337 Munich, Germany; Einheit für Klinische Pharmakologie (EKLiP), Helmholtz Zentrum München, German Research Center for Environmental Health (HMGU), 85764 Neuherberg, Germany; Center for Translational Cancer Research (DKTK), Partner Site Munich, 80336 Munich, Germany. Electronic address: sebastian.kobold@med.uni-muenchen.de.
Jazyk:	angličtina
Zdroj:	Immunity [Immunity] 2023 Jan 10; Vol. 56 (1), pp. 143-161.e11.
DOI:	10.1016/j.immuni.2022.12.010
Abstrakt:	Although T cells can exert potent anti-tumor immunity, a subset of T helper (Th) cells producing interleukin-22 (IL-22) in breast and lung tumors is linked to dismal patient outcome. Here, we examined the mechanisms whereby these T cells contribute to disease. In murine models of lung and breast cancer, constitutional and T cell-specific deletion of Il22 reduced metastases without affecting primary tumor growth. Deletion of the IL-22 receptor on cancer cells decreases metastasis to a degree similar to that seen in IL-22-deficient mice. IL-22 induced high expression of CD155, which bound to the activating receptor CD226 on NK cells. Excessive activation led to decreased amounts of CD226 and functionally impaired NK cells, which elevated the metastatic burden. IL-22 signaling was also associated with CD155 expression in human datasets and with poor patient outcomes. Taken together, our findings reveal an immunosuppressive circuit activated by T cell-derived IL-22 that promotes lung metastasis. Competing Interests: Declaration of interests S.K. has received honoraria from TCR2 Inc., Novartis, BMS, and GSK. S.K. and S.E. are inventors of several patents in the field of immuno-oncology. S.K. and S.E. received license fees from TCR2 Inc. and Carina Biotech. S.K. and S.E. received research support from TCR2 Inc., Tabby Therapeutics, Plectonic GmBH, and Arcus Bioscience for work unrelated to the manuscript. (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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