Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer

Although immune-based therapies have revolutionized the management of cancer, novel approaches are urgently needed to improve their outcome. We investigated the role of endogenous steroids in the resistance to cancer immunotherapy, as these have strong immunomodulatory functions. Using a publicly av...

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Main Authors: Hélène Poinot, Eloïse Dupuychaffray, Grégoire Arnoux, Montserrat Alvarez, Jérémie Tachet, Ounss Ezzar, Jonathan Moore, Olivia Bejuy, Eulalia Olesti, Gioele Visconti, Víctor González-Ruiz, Serge Rudaz, Jean-Christophe Tille, Clarissa D. Voegel, Patrycja Nowak-Sliwinska, Carole Bourquin, Aurélien Pommier
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:OncoImmunology
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Online Access:https://www.tandfonline.com/doi/10.1080/2162402X.2023.2286820
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author Hélène Poinot
Eloïse Dupuychaffray
Grégoire Arnoux
Montserrat Alvarez
Jérémie Tachet
Ounss Ezzar
Jonathan Moore
Olivia Bejuy
Eulalia Olesti
Gioele Visconti
Víctor González-Ruiz
Serge Rudaz
Jean-Christophe Tille
Clarissa D. Voegel
Patrycja Nowak-Sliwinska
Carole Bourquin
Aurélien Pommier
author_facet Hélène Poinot
Eloïse Dupuychaffray
Grégoire Arnoux
Montserrat Alvarez
Jérémie Tachet
Ounss Ezzar
Jonathan Moore
Olivia Bejuy
Eulalia Olesti
Gioele Visconti
Víctor González-Ruiz
Serge Rudaz
Jean-Christophe Tille
Clarissa D. Voegel
Patrycja Nowak-Sliwinska
Carole Bourquin
Aurélien Pommier
author_sort Hélène Poinot
collection DOAJ
description Although immune-based therapies have revolutionized the management of cancer, novel approaches are urgently needed to improve their outcome. We investigated the role of endogenous steroids in the resistance to cancer immunotherapy, as these have strong immunomodulatory functions. Using a publicly available database, we found that the intratumoral expression of 11 beta-hydroxysteroid dehydrogenase type 1 (HSD11B1), which regenerates inactive glucocorticoids into active glucocorticoids, was associated with poor clinical outcome and correlated with immunosuppressive gene signatures in patients with renal cell carcinoma (RCC). HSD11B1 was mainly expressed in tumor-infiltrating immune myeloid cells as seen by immunohistochemistry in RCC patient samples. Using peripheral blood mononuclear cells from healthy donors or immune cells isolated from the tumor of RCC patients, we showed that the pharmacological inhibition of HSD11B1 improved the response to the immune checkpoint inhibitor anti-PD-1. In a subcutaneous mouse model of renal cancer, the combination of an HSD11B1 inhibitor with anti-PD-1 treatment increased the proportion of tumor-infiltrating dendritic cells. In an intrarenal mouse tumor model, HSD11B1 inhibition increased the survival of mice treated with anti-PD-1. In addition, inhibition of HSD11B1 sensitized renal tumors in mice to immunotherapy with resiquimod, a Toll-like receptor 7 agonist. Mechanistically, we demonstrated that HSD11B1 inhibition combined with resiquimod increased T cell-mediated cytotoxicity to tumor cells by stimulating the antigen-presenting capacity of dendritic cells. In conclusion, these results support the use of HSD11B1 inhibitors to improve the outcome of immunotherapy in renal cancer and highlight the role of the endogenous glucocorticoid metabolism in the efficacy of immunotherapy.
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spelling doaj-art-419652ef65f04df7a05ec68d586aacf12024-12-03T13:49:34ZengTaylor & Francis GroupOncoImmunology2162-402X2024-12-0113110.1080/2162402X.2023.2286820Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancerHélène Poinot0Eloïse Dupuychaffray1Grégoire Arnoux2Montserrat Alvarez3Jérémie Tachet4Ounss Ezzar5Jonathan Moore6Olivia Bejuy7Eulalia Olesti8Gioele Visconti9Víctor González-Ruiz10Serge Rudaz11Jean-Christophe Tille12Clarissa D. Voegel13Patrycja Nowak-Sliwinska14Carole Bourquin15Aurélien Pommier16School of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandDepartment of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandTranslational Research Centre in Oncohaematology, Faculty of Medicine, University of Geneva, Geneva, SwitzerlandCIBM Center for Biomedical Imaging, Faculty of Medicine, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandDivision of Clinical Pathology, Geneva University Hospitals, Geneva, SwitzerlandDepartment of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandSchool of Pharmaceutical Sciences, University of Geneva, Geneva, SwitzerlandAlthough immune-based therapies have revolutionized the management of cancer, novel approaches are urgently needed to improve their outcome. We investigated the role of endogenous steroids in the resistance to cancer immunotherapy, as these have strong immunomodulatory functions. Using a publicly available database, we found that the intratumoral expression of 11 beta-hydroxysteroid dehydrogenase type 1 (HSD11B1), which regenerates inactive glucocorticoids into active glucocorticoids, was associated with poor clinical outcome and correlated with immunosuppressive gene signatures in patients with renal cell carcinoma (RCC). HSD11B1 was mainly expressed in tumor-infiltrating immune myeloid cells as seen by immunohistochemistry in RCC patient samples. Using peripheral blood mononuclear cells from healthy donors or immune cells isolated from the tumor of RCC patients, we showed that the pharmacological inhibition of HSD11B1 improved the response to the immune checkpoint inhibitor anti-PD-1. In a subcutaneous mouse model of renal cancer, the combination of an HSD11B1 inhibitor with anti-PD-1 treatment increased the proportion of tumor-infiltrating dendritic cells. In an intrarenal mouse tumor model, HSD11B1 inhibition increased the survival of mice treated with anti-PD-1. In addition, inhibition of HSD11B1 sensitized renal tumors in mice to immunotherapy with resiquimod, a Toll-like receptor 7 agonist. Mechanistically, we demonstrated that HSD11B1 inhibition combined with resiquimod increased T cell-mediated cytotoxicity to tumor cells by stimulating the antigen-presenting capacity of dendritic cells. In conclusion, these results support the use of HSD11B1 inhibitors to improve the outcome of immunotherapy in renal cancer and highlight the role of the endogenous glucocorticoid metabolism in the efficacy of immunotherapy.https://www.tandfonline.com/doi/10.1080/2162402X.2023.2286820GlucocorticoidsHSD11B1immunotherapyrenal cancersteroidogenesis
spellingShingle Hélène Poinot
Eloïse Dupuychaffray
Grégoire Arnoux
Montserrat Alvarez
Jérémie Tachet
Ounss Ezzar
Jonathan Moore
Olivia Bejuy
Eulalia Olesti
Gioele Visconti
Víctor González-Ruiz
Serge Rudaz
Jean-Christophe Tille
Clarissa D. Voegel
Patrycja Nowak-Sliwinska
Carole Bourquin
Aurélien Pommier
Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer
OncoImmunology
Glucocorticoids
HSD11B1
immunotherapy
renal cancer
steroidogenesis
title Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer
title_full Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer
title_fullStr Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer
title_full_unstemmed Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer
title_short Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer
title_sort activation of endogenous glucocorticoids by hsd11b1 inhibits the antitumor immune response in renal cancer
topic Glucocorticoids
HSD11B1
immunotherapy
renal cancer
steroidogenesis
url https://www.tandfonline.com/doi/10.1080/2162402X.2023.2286820
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