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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)

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Open Access Green as soon as Postprint is submitted to ZB.

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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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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Cd155 ; Cd226 ; Nk Cells ; Pvr ; T Helper ; Breast Carcinoma ; Interleukin-22 ; Lung Adenocarcinoma ; Metastasis ; Poliovirus Receptor

ISSN (print) / ISBN 1074-7613

e-ISSN 1097-4180

Journal Immunity

Quellenangaben Volume: 56, Issue: 1, Pages: 143-161.e11

Publisher Cell Press

Publishing Place Cambridge, Mass.

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Unit for Clinical Pharmacology (KKG-EKLiP)

Grants 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)