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2. Correction to: Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Mortera, Stefano Levi, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Published
2022
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3. Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Levi Mortera, Stefano, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Published
2021
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4. Data from Integrated Multiomic Profiling Identifies the Epigenetic Regulator PRC2 as a Therapeutic Target to Counteract Leukemia Immune Escape and Relapse

Author

Gambacorta, Valentina, primary, Beretta, Stefano, primary, Ciccimarra, Martina, primary, Zito, Laura, primary, Giannetti, Kety, primary, Andrisani, Angela, primary, Gnani, Daniela, primary, Zanotti, Lucia, primary, Oliveira, Giacomo, primary, Carrabba, Matteo Giovanni, primary, Cittaro, Davide, primary, Merelli, Ivan, primary, Ciceri, Fabio, primary, Di Micco, Raffaella, primary, and Vago, Luca, primary

Published
2023
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5. Myelomonocytic cells in giant cell arteritis activate trained immunity programs sustaining inflammation and cytokine production

Author

Cantoni, Eleonora, primary, Merelli, Ivan, additional, Stefanoni, Davide, additional, Tomelleri, Alessandro, additional, Campochiaro, Corrado, additional, Giordano, Vito, additional, Panigada, Maddalena, additional, Baldissera, Elena M, additional, Merlo Pich, Laura, additional, Natoli, Valentina, additional, Ziogas, Athanasios, additional, Domínguez-Andrés, Jorge, additional, De Luca, Giacomo, additional, Mazza, Davide, additional, Zambrano, Samuel, additional, Gnani, Daniela, additional, Ferrarini, Marina, additional, Ferrero, Elisabetta, additional, Agresti, Alessandra, additional, Vergani, Barbara, additional, Leone, Biagio Eugenio, additional, Cenci, Simone, additional, Ravelli, Angelo, additional, Matucci-Cerinic, Marco, additional, D’Alessandro, Angelo, additional, Joosten, Leo A B, additional, Dagna, Lorenzo, additional, Netea, Mihai G, additional, Molteni, Raffaella, additional, and Cavalli, Giulio, additional

Published
2023
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6. Myelomonocytic cells in giant cell arteritis activate trained immunity programs sustaining inflammation and cytokine production

Author

Cantoni, E, Merelli, I, Stefanoni, D, Tomelleri, A, Campochiaro, C, Giordano, V, Panigada, M, Baldissera, E, Merlo Pich, L, Natoli, V, Ziogas, A, Domínguez-Andrés, J, De Luca, G, Mazza, D, Zambrano, S, Gnani, D, Ferrarini, M, Ferrero, E, Agresti, A, Vergani, B, Leone, B, Cenci, S, Ravelli, A, Matucci-Cerinic, M, D'Alessandro, A, Joosten, L, Dagna, L, Netea, M, Molteni, R, Cavalli, G, Cantoni, Eleonora, Merelli, Ivan, Stefanoni, Davide, Tomelleri, Alessandro, Campochiaro, Corrado, Giordano, Vito, Panigada, Maddalena, Baldissera, Elena M, Merlo Pich, Laura, Natoli, Valentina, Ziogas, Athanasios, Domínguez-Andrés, Jorge, De Luca, Giacomo, Mazza, Davide, Zambrano, Samuel, Gnani, Daniela, Ferrarini, Marina, Ferrero, Elisabetta, Agresti, Alessandra, Vergani, Barbara, Leone, Biagio Eugenio, Cenci, Simone, Ravelli, Angelo, Matucci-Cerinic, Marco, D'Alessandro, Angelo, Joosten, Leo A B, Dagna, Lorenzo, Netea, Mihai G, Molteni, Raffaella, Cavalli, Giulio, Cantoni, E, Merelli, I, Stefanoni, D, Tomelleri, A, Campochiaro, C, Giordano, V, Panigada, M, Baldissera, E, Merlo Pich, L, Natoli, V, Ziogas, A, Domínguez-Andrés, J, De Luca, G, Mazza, D, Zambrano, S, Gnani, D, Ferrarini, M, Ferrero, E, Agresti, A, Vergani, B, Leone, B, Cenci, S, Ravelli, A, Matucci-Cerinic, M, D'Alessandro, A, Joosten, L, Dagna, L, Netea, M, Molteni, R, Cavalli, G, Cantoni, Eleonora, Merelli, Ivan, Stefanoni, Davide, Tomelleri, Alessandro, Campochiaro, Corrado, Giordano, Vito, Panigada, Maddalena, Baldissera, Elena M, Merlo Pich, Laura, Natoli, Valentina, Ziogas, Athanasios, Domínguez-Andrés, Jorge, De Luca, Giacomo, Mazza, Davide, Zambrano, Samuel, Gnani, Daniela, Ferrarini, Marina, Ferrero, Elisabetta, Agresti, Alessandra, Vergani, Barbara, Leone, Biagio Eugenio, Cenci, Simone, Ravelli, Angelo, Matucci-Cerinic, Marco, D'Alessandro, Angelo, Joosten, Leo A B, Dagna, Lorenzo, Netea, Mihai G, Molteni, Raffaella, and Cavalli, Giulio

Abstract

Objective: Trained immunity (TI) is a de facto memory program of innate immune cells, characterized by immunometabolic and epigenetic changes sustaining enhanced production of cytokines. TI evolved as a protective mechanism against infections; however, inappropriate activation can cause detrimental inflammation and might be implicated in the pathogenesis of chronic inflammatory diseases. In this study, we investigated the role of TI in the pathogenesis of giant cell arteritis (GCA), a large-vessel vasculitis characterized by aberrant macrophage activation and excess cytokine production. Methods: Monocytes from GCA patients and from age- and sex-matched healthy donors were subjected to polyfunctional studies, including cytokine production assays at baseline and following stimulation, intracellular metabolomics, chromatin immunoprecipitation-qPCR, and combined ATAC/RNA sequencing. Immunometabolic activation (i.e. glycolysis) was assessed in inflamed vessels of GCA patients with FDG-PET and immunohistochemistry (IHC), and the role of this pathway in sustaining cytokine production was confirmed with selective pharmacologic inhibition in GCA monocytes. Results: GCA monocytes exhibited hallmark molecular features of TI. Specifically, these included enhanced IL-6 production upon stimulation, typical immunometabolic changes (e.g. increased glycolysis and glutaminolysis) and epigenetic changes promoting enhanced transcription of genes governing pro-inflammatory activation. Immunometabolic changes of TI (i.e. glycolysis) were a feature of myelomonocytic cells in GCA lesions and were required for enhanced cytokine production. Conclusions: Myelomonocytic cells in GCA activate TI programs sustaining enhanced inflammatory activation with excess cytokine production.

Published
2023

7. Chromatin organization drives the exploration strategy of nuclear factors

Author

Mazzocca, Matteo, primary, Loffreda, Alessia, additional, Colombo, Emanuele, additional, Fillot, Tom, additional, Gnani, Daniela, additional, Falletta, Paola, additional, Monteleone, Emanuele, additional, Capozi, Serena, additional, Bertrand, Edouard, additional, Legube, Gaelle, additional, Lavagnino, Zeno, additional, Tacchetti, Carlo, additional, and Mazza, Davide, additional

Published
2022
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8. Abstract LB563: Integrated multiomic profiling identifies the epigenetic regulator PRC2 as a therapeutic target to counteract leukemia immune escape and relapse

Author

Gambacorta, Valentina, primary, Beretta, Stefano, additional, Ciccimarra, Martina, additional, Zito, Laura, additional, Giannetti, Kety, additional, Andrisani, Angela, additional, Gnani, Daniela, additional, Zanotti, Lucia, additional, Oliveira, Giacomo, additional, Carrabba, Matteo G., additional, Cittaro, Davide, additional, Merelli, Ivan, additional, Ciceri, Fabio, additional, Di Micco, Raffaella, additional, and Vago, Luca, additional

Published
2022
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9. Integrated Multiomic Profiling Identifies the Epigenetic Regulator PRC2 as a Therapeutic Target to Counteract Leukemia Immune Escape and Relapse

Author

Gambacorta, Valentina, primary, Beretta, Stefano, additional, Ciccimarra, Martina, additional, Zito, Laura, additional, Giannetti, Kety, additional, Andrisani, Angela, additional, Gnani, Daniela, additional, Zanotti, Lucia, additional, Oliveira, Giacomo, additional, Carrabba, Matteo Giovanni, additional, Cittaro, Davide, additional, Merelli, Ivan, additional, Ciceri, Fabio, additional, Di Micco, Raffaella, additional, and Vago, Luca, additional

Published
2022
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10. Additional file 2 of Correction to: Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Mortera, Stefano Levi, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
Data_FILES
Abstract

Additional file 7.

Published
2022
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11. Additional file 1 of Correction to: Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Mortera, Stefano Levi, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
Data_FILES
Abstract

Additional file 6.

Published
2022
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12. Additional file 3 of Correction to: Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects

Author

Romito, Ilaria, Porru, Manuela, Braghini, Maria Rita, Pompili, Luca, Panera, Nadia, Crudele, Annalisa, Gnani, Daniela, De Stefanis, Cristiano, Scarsella, Marco, Pomella, Silvia, Mortera, Stefano Levi, de Billy, Emmanuel, Conti, Adrian Libenzio, Marzano, Valeria, Putignani, Lorenza, Vinciguerra, Manlio, Balsano, Clara, Pastore, Anna, Rota, Rossella, Tartaglia, Marco, Leonetti, Carlo, and Alisi, Anna

Subjects
Data_FILES
Abstract

Additional file 8.

Published
2022
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13. Oncogene-induced maladaptive activation of trained immunity in the pathogenesis and treatment of Erdheim-Chester disease

Author

Molteni, Raffaella, Biavasco, Riccardo, Stefanoni, Davide, Nemkov, Travis, Domínguez-Andrés, Jorge, Arts, Rob J., Merelli, Ivan, Mazza, Davide, Zambrano, Samuel, Panigada, Maddalena, Cantoni, Eleonora, Tengesdal, Isak W., Maksud, Philippe, Piras, Francesco, Cesana, Daniela, Cassina, Laura, Distefano, Gianfranco, Loffreda, Alessia, Gnani, Daniela, De Luca, Giacomo, Tomelleri, Alessandro, Campochiaro, Corrado, Joosten, Leo A.B., Dinarello, Charles A., Kajaste-Rudnitski, Anna, Haroche, Julien, Cardaci, Simone, Cenci, Simone, Dagna, Lorenzo, Doglioni, Claudio, Ferrarini, Marina, Ferrero, Elisabetta, Boletta, Alessandra, D'Alessandro, Angelo, Montini, Eugenio, Netea, Mihai G., and Cavalli, Giulio

Abstract

Trained immunity (TI) is a proinflammatory program induced in monocyte/macrophages upon sensing of specific pathogens and is characterized by immunometabolic and epigenetic changes that enhance cytokine production. Maladaptive activation of TI (ie, in the absence of infection) may result in detrimental inflammation and development of disease; however, the exact role and extent of inappropriate activation of TI in the pathogenesis of human diseases is undetermined. In this study, we uncovered the oncogene-induced, maladaptive induction of TI in the pathogenesis of a human inflammatory myeloid neoplasm (Erdheim-Chester disease, [ECD]), characterized by the BRAFV600E oncogenic mutation in monocyte/macrophages and excess cytokine production. Mechanistically, myeloid cells expressing BRAFV600E exhibit all molecular features of TI: activation of the AKT/mammalian target of rapamycin signaling axis; increased glycolysis, glutaminolysis, and cholesterol synthesis; epigenetic changes on promoters of genes encoding cytokines; and enhanced cytokine production leading to hyperinflammatory responses. In patients with ECD, effective therapeutic strategies combat this maladaptive TI phenotype; in addition, pharmacologic inhibition of immunometabolic changes underlying TI (ie, glycolysis) effectively dampens cytokine production by myeloid cells. This study revealed the deleterious potential of inappropriate activation of TI in the pathogenesis of human inflammatory myeloid neoplasms and the opportunity for inhibition of TI in conditions characterized by maladaptive myeloid-driven inflammation.

Published
2021
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14. Integrated Multiomic Profiling Identifies the Epigenetic Regulator PRC2 as a Therapeutic Target to Counteract Leukemia Immune Escape and Relapse

Author

Valentina Gambacorta, Stefano Beretta, Martina Ciccimarra, Laura Zito, Kety Giannetti, Angela Andrisani, Daniela Gnani, Lucia Zanotti, Giacomo Oliveira, Matteo Giovanni Carrabba, Davide Cittaro, Ivan Merelli, Fabio Ciceri, Raffaella Di Micco, Luca Vago, Gambacorta, Valentina, Beretta, Stefano, Ciccimarra, Martina, Zito, Laura, Giannetti, Kety, Andrisani, Angela, Gnani, Daniela, Zanotti, Lucia, Oliveira, Giacomo, Carrabba, Matteo Giovanni, Cittaro, Davide, Merelli, Ivan, Ciceri, Fabio, di Micco, Raffaella, and Vago, Luca

Subjects
Leukemia, Myeloid, Acute, Oncology, Recurrence, hemic and lymphatic diseases, Hematopoietic Stem Cell Transplantation, Histocompatibility Antigens Class II, Polycomb Repressive Complex 2, Humans, Tumor Escape, Chromatin, Epigenesis, Genetic
Abstract

Immune escape represents a major driver of acute myeloid leukemia (AML) reemergence after allogeneic hematopoietic cell transplantation (allo-HCT), with up to 40% of relapses prompted by nongenomic loss of HLA class II expression in leukemia cells. By integrative analysis of gene expression, DNA methylation, and chromatin accessibility in paired diagnosis/relapse primary samples and in the respective patient-derived xenografts (PDX), we identify the polycomb repressive complex 2 (PRC2) as a key epigenetic driver of this immune escape modality. We report that loss of expression of HLA class II molecules is accompanied by a PRC2-dependent reduction in chromatin accessibility. Pharmacologic inhibition of PRC2 subunits rescues HLA class II expression in AML relapses in vitro and in vivo, with consequent recovery of leukemia recognition by CD4+ T cells. Our results uncover a novel link between epigenetics and leukemia immune escape, which may rapidly translate into innovative strategies to cure or prevent AML posttransplantation relapse. Significance: Loss of HLA class II expression represents a frequent mechanism of leukemia posttransplantation relapse. Here we identify PRC2 as the main epigenetic driver of this immune escape modality and show that its chemical inhibition can reinstate a proficient graft-versus-leukemia effect, providing an innovative rationale for personalized epigenetic immunotherapies. See related commentary by Köhler and Zeiser, p. 1410. This article is highlighted in the In This Issue feature, p. 1397

Published
2022

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