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2. Modulation of regulatory T cell suppression in tumors through OX40

Author

Burocchi, Alessia

Subjects
616.0797
Abstract

Tumor cells develop numerous mechanisms to escape from the control exerted by the immune system. One of these strategies is the accumulation of regulatory T cells (Treg) within the tumor, which keep effector T cells (Teff) and dendritic cells (DC) in an inactive state. An efficient approach to overcome the inhibitory potential of Treg focuses on OX40, a costimulatory molecule constitutively expressed by Treg and induced in activated Teff. The treatment of mouse transplantable tumor models with the mAb OX86, the agonist of OX40, induces tumor rejection by acting on both these T cell subsets. In this study we investigated the fine cellular mechanisms at the basis of this process, dissecting the effects of OX86 on Treg and on CD4+Foxp3-CD44highCD62LlowOX40+ effector memory T cells (Tem), which represent the most abundant Teff subset in the tumor. Upon OX40 stimulation, Treg are "contra-suppressed" and down-modulate the expression of the transcription factor interferon regulatory factor 1 (IRF1), thus reducing the secretion of IL- 10. Conversely OX86 provides activating stimuli to Tern, which up-regulate CD40L and in turn promote the maturation of DC. OX86 shifts the tumoral milieu from tolerogenic to immunogenic, favoring the activation and migration of DC from the tumor to the draining lymph node (dLN) and the subsequent new CTL induction. The relevance of OX40 in Treg biology goes beyond the modulation of their suppressive abilities. OX40 increases the sensitivity of Treg to IL-2, facilitating the phosphorylation of STAT5 through high level of the mirl55 and low level of SOCS1. The overexpression of miR155 endowed Treg of higher suppressive functions, further enhancing tumor growth. These data clearly remark the key roles exerted by OX40 in influencing Treg and Teff behavior. Understanding how to manipulate OX40 signaling will provide great advantage in the development of efficient therapy for both tumors and autoimmune diseases.

Published
2012
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3. Fig.s3new from Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Checkpoint Inhibitors

Author

Ratti, Chiara, primary, Botti, Laura, primary, Cancila, Valeria, primary, Galvan, Silvia, primary, Torselli, Ilaria, primary, Garofalo, Cecilia, primary, Manara, Maria Cristina, primary, Bongiovanni, Lucia, primary, Valenti, Cesare F., primary, Burocchi, Alessia, primary, Parenza, Mariella, primary, Cappetti, Barbara, primary, Sangaletti, Sabina, primary, Tripodo, Claudio, primary, Scotlandi, Katia, primary, Colombo, Mario P., primary, and Chiodoni, Claudia, primary

Published
2023
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4. Table S1 from Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Checkpoint Inhibitors

Author

Ratti, Chiara, primary, Botti, Laura, primary, Cancila, Valeria, primary, Galvan, Silvia, primary, Torselli, Ilaria, primary, Garofalo, Cecilia, primary, Manara, Maria Cristina, primary, Bongiovanni, Lucia, primary, Valenti, Cesare F., primary, Burocchi, Alessia, primary, Parenza, Mariella, primary, Cappetti, Barbara, primary, Sangaletti, Sabina, primary, Tripodo, Claudio, primary, Scotlandi, Katia, primary, Colombo, Mario P., primary, and Chiodoni, Claudia, primary

Published
2023
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5. Table S2-S3-S4 from Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Checkpoint Inhibitors

Author

Ratti, Chiara, primary, Botti, Laura, primary, Cancila, Valeria, primary, Galvan, Silvia, primary, Torselli, Ilaria, primary, Garofalo, Cecilia, primary, Manara, Maria Cristina, primary, Bongiovanni, Lucia, primary, Valenti, Cesare F., primary, Burocchi, Alessia, primary, Parenza, Mariella, primary, Cappetti, Barbara, primary, Sangaletti, Sabina, primary, Tripodo, Claudio, primary, Scotlandi, Katia, primary, Colombo, Mario P., primary, and Chiodoni, Claudia, primary

Published
2023
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6. Data from Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Checkpoint Inhibitors

Author

Ratti, Chiara, primary, Botti, Laura, primary, Cancila, Valeria, primary, Galvan, Silvia, primary, Torselli, Ilaria, primary, Garofalo, Cecilia, primary, Manara, Maria Cristina, primary, Bongiovanni, Lucia, primary, Valenti, Cesare F., primary, Burocchi, Alessia, primary, Parenza, Mariella, primary, Cappetti, Barbara, primary, Sangaletti, Sabina, primary, Tripodo, Claudio, primary, Scotlandi, Katia, primary, Colombo, Mario P., primary, and Chiodoni, Claudia, primary

Published
2023
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7. Fig.S5 new from Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Checkpoint Inhibitors

Author

Ratti, Chiara, primary, Botti, Laura, primary, Cancila, Valeria, primary, Galvan, Silvia, primary, Torselli, Ilaria, primary, Garofalo, Cecilia, primary, Manara, Maria Cristina, primary, Bongiovanni, Lucia, primary, Valenti, Cesare F., primary, Burocchi, Alessia, primary, Parenza, Mariella, primary, Cappetti, Barbara, primary, Sangaletti, Sabina, primary, Tripodo, Claudio, primary, Scotlandi, Katia, primary, Colombo, Mario P., primary, and Chiodoni, Claudia, primary

Published
2023
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8. Data from Persistent Immune Stimulation Exacerbates Genetically Driven Myeloproliferative Disorders via Stromal Remodeling

Author

Tripodo, Claudio, primary, Burocchi, Alessia, primary, Piccaluga, Pier Paolo, primary, Chiodoni, Claudia, primary, Portararo, Paola, primary, Cappetti, Barbara, primary, Botti, Laura, primary, Gulino, Alessandro, primary, Isidori, Alessandro, primary, Liso, Arcangelo, primary, Visani, Giuseppe, primary, Martelli, Maria Paola, primary, Falini, Brunangelo, primary, Pandolfi, Pier Paolo, primary, Colombo, Mario P., primary, and Sangaletti, Sabina, primary

Published
2023
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9. SupplementarydataREV from Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Checkpoint Inhibitors

Author

Ratti, Chiara, primary, Botti, Laura, primary, Cancila, Valeria, primary, Galvan, Silvia, primary, Torselli, Ilaria, primary, Garofalo, Cecilia, primary, Manara, Maria Cristina, primary, Bongiovanni, Lucia, primary, Valenti, Cesare F., primary, Burocchi, Alessia, primary, Parenza, Mariella, primary, Cappetti, Barbara, primary, Sangaletti, Sabina, primary, Tripodo, Claudio, primary, Scotlandi, Katia, primary, Colombo, Mario P., primary, and Chiodoni, Claudia, primary

Published
2023
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10. Supplementary Methods, Figures, and Tables from Persistent Immune Stimulation Exacerbates Genetically Driven Myeloproliferative Disorders via Stromal Remodeling

Author

Tripodo, Claudio, primary, Burocchi, Alessia, primary, Piccaluga, Pier Paolo, primary, Chiodoni, Claudia, primary, Portararo, Paola, primary, Cappetti, Barbara, primary, Botti, Laura, primary, Gulino, Alessandro, primary, Isidori, Alessandro, primary, Liso, Arcangelo, primary, Visani, Giuseppe, primary, Martelli, Maria Paola, primary, Falini, Brunangelo, primary, Pandolfi, Pier Paolo, primary, Colombo, Mario P., primary, and Sangaletti, Sabina, primary

Published
2023
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11. Data from Osteopontin Shapes Immunosuppression in the Metastatic Niche

Author

Sangaletti, Sabina, primary, Tripodo, Claudio, primary, Sandri, Sara, primary, Torselli, Ilaria, primary, Vitali, Caterina, primary, Ratti, Chiara, primary, Botti, Laura, primary, Burocchi, Alessia, primary, Porcasi, Rossana, primary, Tomirotti, Andrea, primary, Colombo, Mario P., primary, and Chiodoni, Claudia, primary

Published
2023
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17. OX40 triggering concomitant to IL12-engineered cell vaccine hampers the immunoprevention of HER2/neu-driven mammary carcinogenesis

Author

Nanni, Patrizia, primary, De Giovanni, Carla, additional, Burocchi, Alessia, additional, Nicoletti, Giordano, additional, Landuzzi, Lorena, additional, Palladini, Arianna, additional, Ianzano, Marianna Lucia, additional, Arioli, Ivano, additional, Colombo, Mario P., additional, and Lollini, Pier-Luigi, additional

Published
2018
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18. Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Checkpoint Inhibitors

Author

Ratti, Chiara, primary, Botti, Laura, additional, Cancila, Valeria, additional, Galvan, Silvia, additional, Torselli, Ilaria, additional, Garofalo, Cecilia, additional, Manara, Maria Cristina, additional, Bongiovanni, Lucia, additional, Valenti, Cesare F., additional, Burocchi, Alessia, additional, Parenza, Mariella, additional, Cappetti, Barbara, additional, Sangaletti, Sabina, additional, Tripodo, Claudio, additional, Scotlandi, Katia, additional, Colombo, Mario P., additional, and Chiodoni, Claudia, additional

Published
2017
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19. Persistent Immune Stimulation Exacerbates Genetically Driven Myeloproliferative Disorders via Stromal Remodeling

Author

Tripodo, Claudio, primary, Burocchi, Alessia, additional, Piccaluga, Pier Paolo, additional, Chiodoni, Claudia, additional, Portararo, Paola, additional, Cappetti, Barbara, additional, Botti, Laura, additional, Gulino, Alessandro, additional, Isidori, Alessandro, additional, Liso, Arcangelo, additional, Visani, Giuseppe, additional, Martelli, Maria Paola, additional, Falini, Brunangelo, additional, Pandolfi, Pier Paolo, additional, Colombo, Mario P., additional, and Sangaletti, Sabina, additional

Published
2017
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20. Reciprocal influence of B cells and tumor macro and microenvironments in the ApcMin/+ model of colorectal cancer

Author

Mion, Francesca, primary, Vetrano, Stefania, additional, Tonon, Silvia, additional, Valeri, Viviana, additional, Piontini, Andrea, additional, Burocchi, Alessia, additional, Petti, Luciana, additional, Frossi, Barbara, additional, Gulino, Alessandro, additional, Tripodo, Claudio, additional, Colombo, Mario P., additional, and Pucillo, Carlo E., additional

Published
2017
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22. OX40 expression in tumor-associated Tregs as a potential prognostic biomarker and immunotherapeutic target in ovarian cancer.

Author

Di Nicola, Massimo A., primary, Zappasodi, Roberta, additional, Burocchi, Alessia, additional, Ruggiero, Giusi, additional, Rossini, Anna, additional, Martinelli, Fabio, additional, Tripodo, Claudio, additional, Magni, Michele, additional, Lorusso, Domenica, additional, De Braud, Filippo G., additional, Raspagliesi, Francesco, additional, and Colombo, Mario Paolo, additional

Published
2015
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24. Mast Cells Control the Expansion and Differentiation of IL-10–Competent B Cells

Author

Mion, Francesca, primary, D’Incà, Federica, additional, Danelli, Luca, additional, Toffoletto, Barbara, additional, Guarnotta, Carla, additional, Frossi, Barbara, additional, Burocchi, Alessia, additional, Rigoni, Alice, additional, Gerdes, Norbert, additional, Lutgens, Esther, additional, Tripodo, Claudio, additional, Colombo, Mario P., additional, Rivera, Juan, additional, Vitale, Gaetano, additional, and Pucillo, Carlo E., additional

Published
2014
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25. Osteopontin Shapes Immunosuppression in the Metastatic Niche

Author

Sangaletti, Sabina, primary, Tripodo, Claudio, additional, Sandri, Sara, additional, Torselli, Ilaria, additional, Vitali, Caterina, additional, Ratti, Chiara, additional, Botti, Laura, additional, Burocchi, Alessia, additional, Porcasi, Rossana, additional, Tomirotti, Andrea, additional, Colombo, Mario P., additional, and Chiodoni, Claudia, additional

Published
2014
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27. The matricellular protein SPARC supports follicular dendritic cell networking toward Th17 responses

Author

Piconese, Silvia, primary, Costanza, Massimo, additional, Tripodo, Claudio, additional, Sangaletti, Sabina, additional, Musio, Silvia, additional, Pittoni, Paola, additional, Poliani, Pietro L., additional, Burocchi, Alessia, additional, Passafaro, Alfonso L., additional, Gorzanelli, Andrea, additional, Vitali, Caterina, additional, Chiodoni, Claudia, additional, Barnaba, Vincenzo, additional, Pedotti, Rosetta, additional, and Colombo, Mario P., additional

Published
2011
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31. Modulation of regulatory T cell suppression in tumors through OX40

Author

Burocchi, Alessia and Burocchi, Alessia

Abstract

Tumor cells develop numerous mechanisms to escape from the control exerted by the immune system. One of these strategies is the accumulation of regulatory T cells (Treg) within the tumor, which keep effector T cells (Teff) and dendritic cells (DC) in an inactive state. An efficient approach to overcome the inhibitory potential of Treg focuses on OX40, a costimulatory molecule constitutively expressed by Treg and induced in activated Teff. The treatment of mouse transplantable tumor models with the mAb OX86, the agonist of OX40, induces tumor rejection by acting on both these T cell subsets. In this study we investigated the fine cellular mechanisms at the basis of this process, dissecting the effects of OX86 on Treg and on CD4+Foxp3-CD44highCD62LlowOX40+ effector memory T cells (Tem), which represent the most abundant Teff subset in the tumor. Upon OX40 stimulation, Treg are "contra-suppressed" and down-modulate the expression of the transcription factor interferon regulatory factor 1 (IRF1), thus reducing the secretion of IL- 10. Conversely OX86 provides activating stimuli to Tern, which up-regulate CD40L and in turn promote the maturation of DC. OX86 shifts the tumoral milieu from tolerogenic to immunogenic, favoring the activation and migration of DC from the tumor to the draining lymph node (dLN) and the subsequent new CTL induction. The relevance of OX40 in Treg biology goes beyond the modulation of their suppressive abilities. OX40 increases the sensitivity of Treg to IL-2, facilitating the phosphorylation of STAT5 through high level of the mirl55 and low level of SOCS1. The overexpression of miR155 endowed Treg of higher suppressive functions, further enhancing tumor growth. These data clearly remark the key roles exerted by OX40 in influencing Treg and Teff behavior. Understanding how to manipulate OX40 signaling will provide great advantage in the development of efficient therapy for

32. Modulation of regulatory T cell suppression in tumors through OX40

Author

Burocchi, Alessia and Burocchi, Alessia

Abstract

Tumor cells develop numerous mechanisms to escape from the control exerted by the immune system. One of these strategies is the accumulation of regulatory T cells (Treg) within the tumor, which keep effector T cells (Teff) and dendritic cells (DC) in an inactive state. An efficient approach to overcome the inhibitory potential of Treg focuses on OX40, a costimulatory molecule constitutively expressed by Treg and induced in activated Teff. The treatment of mouse transplantable tumor models with the mAb OX86, the agonist of OX40, induces tumor rejection by acting on both these T cell subsets. In this study we investigated the fine cellular mechanisms at the basis of this process, dissecting the effects of OX86 on Treg and on CD4+Foxp3-CD44highCD62LlowOX40+ effector memory T cells (Tem), which represent the most abundant Teff subset in the tumor. Upon OX40 stimulation, Treg are "contra-suppressed" and down-modulate the expression of the transcription factor interferon regulatory factor 1 (IRF1), thus reducing the secretion of IL- 10. Conversely OX86 provides activating stimuli to Tern, which up-regulate CD40L and in turn promote the maturation of DC. OX86 shifts the tumoral milieu from tolerogenic to immunogenic, favoring the activation and migration of DC from the tumor to the draining lymph node (dLN) and the subsequent new CTL induction. The relevance of OX40 in Treg biology goes beyond the modulation of their suppressive abilities. OX40 increases the sensitivity of Treg to IL-2, facilitating the phosphorylation of STAT5 through high level of the mirl55 and low level of SOCS1. The overexpression of miR155 endowed Treg of higher suppressive functions, further enhancing tumor growth. These data clearly remark the key roles exerted by OX40 in influencing Treg and Teff behavior. Understanding how to manipulate OX40 signaling will provide great advantage in the development of efficient therapy for

33. Reciprocal influence of B cells and tumor macro and microenvironments in the ApcMin/+model of colorectal cancer

Author

Mion, Francesca, Vetrano, Stefania, Tonon, Silvia, Valeri, Viviana, Piontini, Andrea, Burocchi, Alessia, Petti, Luciana, Frossi, Barbara, Gulino, Alessandro, Tripodo, Claudio, Colombo, Mario P., and Pucillo, Carlo E.

Abstract

ABSTRACTOne of the most fascinating aspects of the immune system is its dynamism, meant as the ability to change and readapt according to the organism needs. Following an insult, we assist to the spontaneous organization of different immune cells which cooperate, locally and at distance, to build up an appropriate response. Throughout tumor progression, adaptations within the systemic tumor environment, or macroenvironment, result in the promotion of tumor growth, tumor invasion and metastasis to distal organs, but also to dramatic changes in the activity and composition of the immune system. In this work, we show the changes of the B-cell arm of the immune system following tumor progression in the ApcMin/+model of colorectal cancer. Tumor macroenvironment leads to an increased proportion of total and IL-10-competent B cells in draining LNs while activates a differentiation route that leads to the expansion of IgA+lymphocytes in the spleen and peritoneum. Importantly, serum IgA levels were significantly higher in ApcMin/+than Wt mice. The peculiar involvement of IgA response in the adenomatous transformation had correlates in the gut-mucosal compartment where IgA-positive elements increased from normal mucosa to areas of low grade dysplasia while decreasing upon overt carcinomatous transformation. Altogether, our findings provide a snapshot of the tumor education of B lymphocytes in the ApcMin/+model of colorectal cancer. Understanding how tumor macroenvironment affects the differentiation, function and distribution of B lymphocytes is pivotal to the generation of specific therapies, targeted to switching B cells to an anti-, rather than pro-, tumoral phenotype.

Published
2017
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34. Persistent immune stimulation exacerbates genetically driven myeloproliferative disorders via stromal remodeling

Author

Maria Paola Martelli, Claudia Chiodoni, Barbara Cappetti, Pier Paolo Piccaluga, Mario P. Colombo, Brunangelo Falini, Pier Paolo Pandolfi, Alessandro Isidori, Alessandro Gulino, Arcangelo Liso, Giuseppe Visani, Paola Portararo, Alessia Burocchi, Sabina Sangaletti, Claudio Tripodo, Laura Botti, Tripodo, Claudio, Burocchi, Alessia, Piccaluga, Pier Paolo, Chiodoni, Claudia, Portararo, Paola, Cappetti, Barbara, Botti, Laura, Gulino, Alessandro, Isidori, Alessandro, Liso, Arcangelo, Visani, Giuseppe, Martelli, Maria Paola, Falini, Brunangelo, Pandolfi, Pier Paolo, Colombo, Mario P., and Sangaletti, Sabina

Subjects
0301 basic medicine, Cancer Research, Stromal cell, Myeloid, Mice, Transgenic, Vascular Remodeling, Biology, Inbred C57BL, Transgenic, Mice, 03 medical and health sciences, Myelogenous, Myeloproliferative Disorders, medicine, Animals, Humans, Myeloproliferative Disorder, Cell Proliferation, Mice, Inbred C57BL, Mice, Inbred CBA, Stromal Cells, Oncology, Animal, Stromal Cell, Inbred CBA, Neutrophil extracellular traps, medicine.disease, Haematopoiesis, Leukemia, 030104 developmental biology, medicine.anatomical_structure, Immunology, Bone marrow, Nucleophosmin, Human
Abstract

Systemic immune stimulation has been associated with increased risk of myeloid malignancies, but the pathogenic link is unknown. We demonstrate in animal models that experimental systemic immune activation alters the bone marrow stromal microenvironment, disarranging extracellular matrix (ECM) microarchitecture, with downregulation of secreted protein acidic and rich in cysteine (SPARC) and collagen-I and induction of complement activation. These changes were accompanied by a decrease in Treg frequency and by an increase in activated effector T cells. Under these conditions, hematopoietic precursors harboring nucleophosmin-1 (NPM1) mutation generated myeloid cells unfit for normal hematopoiesis but prone to immunogenic death, leading to neutrophil extracellular trap (NET) formation. NET fostered the progression of the indolent NPM1-driven myeloproliferation toward an exacerbated and proliferative dysplastic phenotype. Enrichment in NET structures was found in the bone marrow of patients with autoimmune disorders and in NPM1-mutated acute myelogenous leukemia (AML) patients. Genes involved in NET formation in the animal model were used to design a NET-related inflammatory gene signature for human myeloid malignancies. This signature identified two AML subsets with different genetic complexity and different enrichment in NPM1 mutation and predicted the response to immunomodulatory drugs. Our results indicate that stromal/ECM changes and priming of bone marrow NETosis by systemic inflammatory conditions can complement genetic and epigenetic events towards the development and progression of myeloid malignancy. Cancer Res; 77(13); 3685–99. ©2017 AACR.

Published
2017

35. OX40 triggering concomitant to IL12-engineered cell vaccine hampers the immunoprevention of HER2/neu-driven mammary carcinogenesis

Author

Pier Luigi Lollini, Marianna L. Ianzano, Arianna Palladini, Mario P. Colombo, Lorena Landuzzi, Patrizia Nanni, Carla De Giovanni, Alessia Burocchi, Ivano Arioli, Giordano Nicoletti, Nanni, Patrizia, De Giovanni, Carla, Burocchi, Alessia, Nicoletti, Giordano, Landuzzi, Lorena, Palladini, Arianna, Ianzano, Marianna Lucia, Arioli, Ivano, Colombo, Mario P., and Lollini, Pier-Luigi

Subjects
lcsh:Immunologic diseases. Allergy, 0301 basic medicine, Immunology, Cell, lcsh:RC254-282, HER2/neu, 03 medical and health sciences, immunoprevention, 0302 clinical medicine, mammary cancer, Cancer Vaccine, OX40, HER2/neu, Immunoprevention, Mammary cancer, Immunology and Allergy, Medicine, Original Research, biology, business.industry, ox40, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Vaccine efficacy, Histocompatibility, Vaccination, Interleukin 10, 030104 developmental biology, medicine.anatomical_structure, Oncology, her2/neu, 030220 oncology & carcinogenesis, biology.protein, Cancer research, Cancer vaccine, Antibody, cancer vaccine, lcsh:RC581-607, business
Abstract

This study evaluated the effects of combining an OX40 agonistic antibody (aOX40) with a cell vaccine targeting HER2/neu, called “Triplex”. Such HER2/neu cell vaccine included two biological adjuvants (interleukin 12 (IL12) and allogeneic histocompatibility antigens) and was previously found able to prevent autochthonous HER2/neu-driven mammary carcinogenesis. Timing of aOX40 administration, concomitantly or after cell vaccination, gave opposite results. Unexpectedly, vaccine efficacy was hampered by concomitant OX40 triggering. Such decreased immunoprevention was likely due to a reduced induction of anti-HER2/neu antibodies and to a higher level of Treg activation. On the contrary, aOX40 administration after the completion of vaccination slightly but significantly increased immunopreventive vaccine efficacy, and led to increased production of GM-CSF and IL10. In conclusion, OX40 triggering can either impair or ameliorate immunoprevention of HER2/neu-driven mammary carcinogenesis depending on the schedule of aOX40 administration.

Published
2018
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36. Reciprocal influence of B cells and tumor macro and microenvironments in the ApcMin/+ model of colorectal cancer

Author

Alessia Burocchi, Francesca Mion, Luciana Petti, Mario P. Colombo, Stefania Vetrano, Barbara Frossi, Silvia Tonon, Alessandro Gulino, Andrea Piontini, Carlo Pucillo, Claudio Tripodo, Viviana Valeri, Mion, Francesca, Vetrano, Stefania, Tonon, Silvia, Valeri, Viviana, Piontini, Andrea, Burocchi, Alessia, Petti, Luciana, Frossi, Barbara, Gulino, Alessandro, Tripodo, Claudio, Colombo, Mario P, and Pucillo, Carlo E

Subjects
lcsh:Immunologic diseases. Allergy, 0301 basic medicine, Colorectal cancer, Immunology, Spleen, intestinal cancer, Biology, lcsh:RC254-282, Metastasis, 03 medical and health sciences, Immune system, Peritoneum, medicine, Immunology and Allergy, apcmin/+ mice, ApcMin/+mice, B lymphocytes, IgA, IL-10, Oncology, B lymphocyte, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, Phenotype, Interleukin 10, 030104 developmental biology, medicine.anatomical_structure, Tumor progression, b lymphocytes, lcsh:RC581-607
Abstract

One of the most fascinating aspects of the immune system is its dynamism, meant as the ability to change and readapt according to the organism needs. Following an insult, we assist to the spontaneous organization of different immune cells which cooperate, locally and at distance, to build up an appropriate response. Throughout tumor progression, adaptations within the systemic tumor environment, or macroenvironment, result in the promotion of tumor growth, tumor invasion and metastasis to distal organs, but also to dramatic changes in the activity and composition of the immune system. In this work, we show the changes of the B-cell arm of the immune system following tumor progression in the ApcMin/+ model of colorectal cancer. Tumor macroenvironment leads to an increased proportion of total and IL-10-competent B cells in draining LNs while activates a differentiation route that leads to the expansion of IgA+ lymphocytes in the spleen and peritoneum. Importantly, serum IgA levels were significantly higher in ApcMin/+ than Wt mice. The peculiar involvement of IgA response in the adenomatous transformation had correlates in the gut-mucosal compartment where IgA-positive elements increased from normal mucosa to areas of low grade dysplasia while decreasing upon overt carcinomatous transformation. Altogether, our findings provide a snapshot of the tumor education of B lymphocytes in the ApcMin/+ model of colorectal cancer. Understanding how tumor macroenvironment affects the differentiation, function and distribution of B lymphocytes is pivotal to the generation of specific therapies, targeted to switching B cells to an anti-, rather than pro-, tumoral phenotype.

Published
2017
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37. Reciprocal influence of B cells and tumor macro and microenvironments in the Apc Min/+ model of colorectal cancer.

Author

Mion F, Vetrano S, Tonon S, Valeri V, Piontini A, Burocchi A, Petti L, Frossi B, Gulino A, Tripodo C, Colombo MP, and Pucillo CE

Abstract

One of the most fascinating aspects of the immune system is its dynamism, meant as the ability to change and readapt according to the organism needs. Following an insult, we assist to the spontaneous organization of different immune cells which cooperate, locally and at distance, to build up an appropriate response. Throughout tumor progression, adaptations within the systemic tumor environment, or macroenvironment, result in the promotion of tumor growth, tumor invasion and metastasis to distal organs, but also to dramatic changes in the activity and composition of the immune system. In this work, we show the changes of the B-cell arm of the immune system following tumor progression in the Apc Min/+ model of colorectal cancer. Tumor macroenvironment leads to an increased proportion of total and IL-10-competent B cells in draining LNs while activates a differentiation route that leads to the expansion of IgA + lymphocytes in the spleen and peritoneum. Importantly, serum IgA levels were significantly higher in Apc Min/+ than Wt mice. The peculiar involvement of IgA response in the adenomatous transformation had correlates in the gut-mucosal compartment where IgA-positive elements increased from normal mucosa to areas of low grade dysplasia while decreasing upon overt carcinomatous transformation. Altogether, our findings provide a snapshot of the tumor education of B lymphocytes in the Apc Min/+ model of colorectal cancer. Understanding how tumor macroenvironment affects the differentiation, function and distribution of B lymphocytes is pivotal to the generation of specific therapies, targeted to switching B cells to an anti-, rather than pro-, tumoral phenotype.

Published
2017
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