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Briukhovetska, D.* ; Suarez-Gosalvez, J.* ; Voigt, C.* ; Markota, A.* ; Giannou, A.D.* ; Schübel, M.* ; Jobst, J.* ; Zhang, T.* ; Dörr, J.* ; Märkl, F.* ; Majed, L.* ; Müller, P.J.* ; May, P.* ; Gottschlich, A.* ; Tokarew, N.* ; Lücke, J.* ; Oner, A.* ; Schwerdtfeger, M.* ; Andreu-Sanz, D.* ; Grünmeier, R.* ; Seifert, M.* ; Michaelides, S.* ; Hristov, M.* ; König, L.M.* ; Cadilha, B.L.* ; Mikhaylov, O.* ; Anders, H.J.* ; Rothenfußer, S. ; Flavell, R.A.* ; Cerezo-Wallis, D.* ; Tejedo, C.* ; Soengas, M.S.* ; Bald, T.* ; Huber, S.* ; Endres, S. ; Kobold, S.

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

Immunity 56, 143-161.e11 (2023)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Cd155 ; Cd226 ; Nk Cells ; Pvr ; T Helper ; Breast Carcinoma ; Interleukin-22 ; Lung Adenocarcinoma ; Metastasis ; Poliovirus Receptor
Sprache englisch
Veröffentlichungsjahr 2023
HGF-Berichtsjahr 2023
ISSN (print) / ISBN 1074-7613
e-ISSN 1097-4180
Zeitschrift Immunity
Quellenangaben Band: 56, Heft: 1, Seiten: 143-161.e11 Artikelnummer: , Supplement: ,
Verlag Cell Press
Verlagsort Cambridge, Mass.
Begutachtungsstatus Peer reviewed
Institut(e) Unit for Clinical Pharmacology (KKG-EKLiP)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-522100-001
Förderungen Melanoma Research Alliance
H2020 Program of the European Union
Marie-Sklodowska-Curie Program Training Network for Optimizing Adoptive T Cell Therapy of Cancer - H2020 Program of the European Union
Else Kroner-Fresenius-Stiftung
German Cancer Aid
Wilhelm Sander-Stiftung
Ernst-Jung-Stiftung
Bundesministerium fur Bildung und Forschung
m4 award of the Bavarian Ministry of Economic Affairs
European Research Council
ERC
Deutsche Forschungsgemeinschaft (German Research Foundation, DFG)
International Doctoral Program i-Target: Immunotargeting of Cancer - Elite Network of Bavaria
Hector Foundation
Fritz Bender Foundation
Deutsche Jose Carreras Leukamie-Stiftung
Helmholtz Zentrum Munchen
Neuherberg, Germany
DFG
Novartis - DFG under Germany's Excellence Strategy
Else Kroner Memorial Stipendium
Jung Foundation for Science and Research (Ernst Jung Career Development Award)
DOI 10.1016/j.immuni.2022.12.010
WOS ID 000937038000001
Scopus ID 85146047489
PubMed ID 36630913
Erfassungsdatum 2023-01-17
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