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1. Quorum sensing contributes to activated B cell homeostasis and to prevent autoimmunity

Author

Montaudouin, Caroline, Anson, Marie, Hao, Yi, Duncker, Susanne V., Fernandez, Tahia, Gaudin, Emmanuelle, Ehrenstein, Michael, Kerr, William G., Colle, Jean-Herve, Bruhns, Pierre, Daeron, Marc, and Freitas, Antonio A.

Subjects
Quantitative Biology - Cell Behavior
Abstract

Maintenance of plasma IgM levels is critical for immune system function and homeostasis in humans and mice. However, the mechanisms that control homeostasis of the activated IgM-secreting B cells are unknown. After adoptive transfer into immune-deficient hosts, B-lymphocytes expand poorly but fully reconstitute the pool of natural IgM-secreting cells and circulating IgM levels. By using sequential cell transfers and B cell populations from several mutant mice, we were able to identify novel mechanisms regulating the size of the IgM-secreting B cell pool. Contrary to previous mechanisms described regulating homeostasis, which involve competition for the same niche by cells having overlapping survival requirements, homeostasis of the innate IgM-secreting B cell pool is also achieved when B cells populations are able to monitor the number of activated B cells by detecting their secreted products. Notably, B cell populations are able to assess the density of activated B cells by sensing their secreted IgG. This process involves the Fc{\gamma}RIIB, a low-affinity IgG receptor that is expressed on B cells and acts as a negative regulator of B cell activation, and its intracellular effector the inositol phosphatase SHIP. As a result of the engagement of this inhibitory pathway the number of activated IgM-secreting B cells is kept under control. We hypothesize that malfunction of this quorum-sensing mechanism may lead to uncontrolled B cell activation and autoimmunity., Comment: 34 pages, 5 figures

Published
2012

2. CXCR6 deficiency impairs cancer vaccine efficacy and CD8+ resident memory T-cell recruitment in head and neck and lung tumors

Author

Karaki, Soumaya, Blanc, Charlotte, Tran, Thi, Galy-Fauroux, Isabelle, Mougel, Alice, Dransart, Estelle, Anson, Marie, Tanchot, Corinne, Paolini, Lea, Gruel, Nadege, Gibault, Laure, Lepimpec-Barhes, Francoise, Fabre, Elizabeth, Benhamouda, Nadine, Badoual, Cecile, Damotte, Diane, Donnadieu, Emmanuel, Kobold, Sebastian, Mami-Chouaib, Fathia, Golub, Rachel, Johannes, Ludger, Tartour, Eric, Vougny, Marie-Christine, Université Sorbonne Paris Cité - - USPC2011 - ANR-11-IDEX-0005 - IDEX - VALID, Paris-Centre de Recherche Cardiovasculaire (PARCC (UMR_S 970/ U970)), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Equipe labellisée Ligue contre le Cancer, Chimie biologique des membranes et ciblage thérapeutique (CBMCT - UMR 3666 / U1143), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Unité de génétique et biologie des cancers (U830), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Département de Recherche Translationnelle, Institut Curie [Paris], Service d’anatomo‑pathologie [AP-HP Hôpital Européen Georges Pompidou] (Centre de Ressources biologiques), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Center for Integrated Protein Science (CIPSM), Technische Universität Munchen - Université Technique de Munich [Munich, Allemagne] (TUM)-Ludwig-Maximilians-Universität München (LMU)-Helmholtz Zentrum München = German Research Center for Environmental Health, German Center for Lung Research - DZL [Munich, Germany], Immunologie intégrative des tumeurs et immunothérapie des cancers (INTIM), Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Lymphopoïèse (Lymphopoïèse (UMR_1223 / U1223 / U-Pasteur_4)), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), This work has been funded by Fondation ARC, INCA PLBio, Labex Immuno-Oncology, Site intégré de recherche en cancérologie (SIRIC CARPEM, SIRIC Curie), Cancéropole d’Ile de France, Carnot Curie Cancer, FONCER. SK is supported by the European Research Council (grant 756017, ARMOR-T)., ANR-11-IDEX-0005,USPC,Université Sorbonne Paris Cité(2011), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC), Département de recherche translationnelle, Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Technische Universität Munchen - Université Technique de Munich [Munich, Allemagne] (TUM)-Helmholtz-Zentrum München (HZM)-Ludwig Maximilian University of Munich [Germany] (LMU München), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), École Pratique des Hautes Études (EPHE), and Technical University of Munich (TUM)-Ludwig Maximilian University of Munich [Germany] (LMU München)-Helmholtz-Zentrum München (HZM)

Subjects
Lung Neoplasms, [SDV.IMM] Life Sciences [q-bio]/Immunology, Vaccine Efficacy, immunization, Cancer Vaccines, Memory T Cells, Lymphocytes, Tumor-Infiltrating, Cell Line, Tumor, Tumor Microenvironment, Animals, Humans, Administration, Intranasal, RC254-282, Receptors, CXCR6, Mice, Knockout, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Basic Tumor Immunology, Chemokine CXCL16, adaptive immunity, vaccination, Tumor Burden, Mice, Inbred C57BL, Phenotype, Head and Neck Neoplasms, CD8-positive T-lymphocytes, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Immunologic Memory
Abstract

International audience; Background Resident memory T lymphocytes (TRM) are located in tissues and play an important role in immunosurveillance against tumors. The presence of TRM prior to treatment or their induction is associated to the response to anti-Programmed cell death protein 1 (PD-1)/Programmed death-ligand 1 (PD-L1) immunotherapy and the efficacy of cancer vaccines. Previous work by our group and others has shown that the intranasal route of vaccination allows more efficient induction of these cells in head and neck and lung mucosa, resulting in better tumor protection. The mechanisms of in vivo migration of these cells remains largely unknown, apart from the fact that they express the chemokine receptor CXCR6.Methods We used CXCR6-deficient mice and an intranasal tumor vaccination model targeting the Human Papillomavirus (HPV) E7 protein expressed by the TC-1 lung cancer epithelial cell line. The role of CXCR6 and its ligand, CXCL16, was analyzed using multiparametric cytometric techniques and Luminex assays.Human biopsies obtained from patients with lung cancer were also included in this study.Results We showed that CXCR6 was preferentially expressed by CD8+ TRM after vaccination in mice and also on intratumoral CD8+ TRM derived from human lung cancer. We also demonstrate that vaccination of Cxcr6-deficient mice induces a defect in the lung recruitment of antigen-specific CD8+ T cells, preferentially in the TRM subsets. In addition, we found that intranasal vaccination with a cancer vaccine is less effective in these Cxcr6-deficient mice compared with wild-type mice, and this loss of efficacy is associated with decreased recruitment of local antitumor CD8+ TRM. Interestingly, intranasal, but not intramuscular vaccination induced higher and more sustained concentrations of CXCL16, compared with other chemokines, in the bronchoalveolar lavage fluid and pulmonary parenchyma.Conclusions This work demonstrates the in vivo role of CXCR6-CXCL16 axis in the migration of CD8+ resident memory T cells in lung mucosa after vaccination, resulting in the control of tumor growth. This work reinforces and explains why the intranasal route of vaccination is the most appropriate strategy for inducing these cells in the head and neck and pulmonary mucosa, which remains a major objective to overcome resistance to anti-PD-1/PD-L1, especially in cold tumors.

Published
2021

3. Oncogenic β-catenin triggers an inflammatory response that determines the aggressiveness of hepatocellular carcinoma in mice

Author

Anson, Marie, Crain-Denoyelle, Anne-Marie, Baud, Veronique, Chereau, Fanny, Gougelet, Angelique, Terris, Benoit, Yamagoe, Satoshi, Colnot, Sabine, Viguier, Mireille, Perret, Christine, and Couty, Jean-Pierre

Subjects
Gene expression -- Research, Hepatoma -- Risk factors -- Genetic aspects -- Care and treatment -- Research, Mice -- Usage -- Models, Health care industry
Abstract

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Its pathogenesis is frequently linked to liver inflammation. Gain-of-function mutations in the gene encoding β-catenin are frequent genetic modifications found in human HCCs. Thus, we investigated whether inflammation was a component of β-catenin--induced tumorigenesis using genetically modified mouse models that recapitulated the stages of initiation and progression of this tumoral process. Oncogenic β-catenin signaling was found to induce an inflammatory program in hepatocytes that involved direct transcriptional control by β-catenin and activation of the NF-κB pathway. This led to a specific inflammatory response, the intensity of which determined the degree of tumor aggressiveness. The chemokine-like chemotactic factor leukocyte cell-derived chemotaxin 2 (LECT2) and invariant NKT (iNKT) cells were identified as key interconnected effectors of liver β-catenin--induced inflammation. In genetic deletion models lacking the gene encoding LECT2 or iNKT cells, hepatic β-catenin signaling triggered the formation of highly malignant HCCs with lung metastasis. Thus, our results identify inflammation as a key player in β-catenin--induced liver tumorigenesis. We provide strong evidence that, by activating pro- and antiinflammatory mediators, β-catenin signaling produces an inflammatory microenvironment that has an impact on tumoral development. Our data are consistent with the fact that most β-catenin--activated HCCs are of better prognosis., Introduction Cumulative evidence indicates that chronic inflammatory diseases result in a predisposition to various types of cancers (1), (2). An inflammatory component is present in the microenvironment of most neoplastic [...]

Published
2012
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5. Lect2 Controls Inflammatory Monocytes to Constrain the Growth and Progression of Hepatocellular Carcinoma

Author

L’Hermitte, Antoine, primary, Pham, Sandrine, additional, Cadoux, Mathilde, additional, Couchy, Gabrielle, additional, Caruso, Stefano, additional, Anson, Marie, additional, Crain‐Denoyelle, Anne‐Marie, additional, Celton‐Morizur, Séverine, additional, Yamagoe, Satoshi, additional, Zucman‐Rossi, Jessica, additional, Desdouets, Chantal, additional, and Couty, Jean‐Pierre, additional

Published
2018
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10. Quorum Sensing Contributes to Activated IgM-Secreting B Cell Homeostasis

Author

Montaudouin, Caroline, primary, Anson, Marie, additional, Hao, Yi, additional, Duncker, Susanne V., additional, Fernandez, Tahia, additional, Gaudin, Emmanuelle, additional, Ehrenstein, Michael, additional, Kerr, William G., additional, Colle, Jean-Hervé, additional, Bruhns, Pierre, additional, Daëron, Marc, additional, and Freitas, António A., additional

Published
2013
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13. CXCR6 deficiency impairs cancer vaccine efficacy and CD8 + resident memory T-cell recruitment in head and neck and lung tumors.

Author

Karaki S, Blanc C, Tran T, Galy-Fauroux I, Mougel A, Dransart E, Anson M, Tanchot C, Paolini L, Gruel N, Gibault L, Lepimpec-Barhes F, Fabre E, Benhamouda N, Badoual C, Damotte D, Donnadieu E, Kobold S, Mami-Chouaib F, Golub R, Johannes L, and Tartour E

Subjects
Administration, Intranasal, Animals, CD8-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes metabolism, Cancer Vaccines administration & dosage, Cancer Vaccines immunology, Cell Line, Tumor, Chemokine CXCL16 metabolism, Female, Head and Neck Neoplasms genetics, Head and Neck Neoplasms immunology, Head and Neck Neoplasms metabolism, Humans, Immunologic Memory, Lung Neoplasms genetics, Lung Neoplasms immunology, Lung Neoplasms metabolism, Lymphocytes, Tumor-Infiltrating immunology, Lymphocytes, Tumor-Infiltrating metabolism, Memory T Cells immunology, Memory T Cells metabolism, Mice, Inbred C57BL, Mice, Knockout, Phenotype, Receptors, CXCR6 genetics, Tumor Burden drug effects, Tumor Microenvironment, Vaccination, Mice, CD8-Positive T-Lymphocytes drug effects, Cancer Vaccines pharmacology, Head and Neck Neoplasms drug therapy, Lung Neoplasms drug therapy, Lymphocytes, Tumor-Infiltrating drug effects, Memory T Cells drug effects, Receptors, CXCR6 deficiency, Vaccine Efficacy
Abstract

Background: Resident memory T lymphocytes (T RM ) are located in tissues and play an important role in immunosurveillance against tumors. The presence of T RM prior to treatment or their induction is associated to the response to anti-Programmed cell death protein 1 (PD-1)/Programmed death-ligand 1 (PD-L1) immunotherapy and the efficacy of cancer vaccines. Previous work by our group and others has shown that the intranasal route of vaccination allows more efficient induction of these cells in head and neck and lung mucosa, resulting in better tumor protection. The mechanisms of in vivo migration of these cells remains largely unknown, apart from the fact that they express the chemokine receptor CXCR6., Methods: We used CXCR6 -deficient mice and an intranasal tumor vaccination model targeting the Human Papillomavirus (HPV) E7 protein expressed by the TC-1 lung cancer epithelial cell line. The role of CXCR6 and its ligand, CXCL16, was analyzed using multiparametric cytometric techniques and Luminex assays.Human biopsies obtained from patients with lung cancer were also included in this study., Results: We showed that CXCR6 was preferentially expressed by CD8 + T RM after vaccination in mice and also on intratumoral CD8 + T RM derived from human lung cancer. We also demonstrate that vaccination of Cxcr6-deficient mice induces a defect in the lung recruitment of antigen-specific CD8 + T cells, preferentially in the T RM subsets. In addition, we found that intranasal vaccination with a cancer vaccine is less effective in these Cxcr6 -deficient mice compared with wild-type mice, and this loss of efficacy is associated with decreased recruitment of local antitumor CD8 + T RM . Interestingly, intranasal, but not intramuscular vaccination induced higher and more sustained concentrations of CXCL16, compared with other chemokines, in the bronchoalveolar lavage fluid and pulmonary parenchyma., Conclusions: This work demonstrates the in vivo role of CXCR6-CXCL16 axis in the migration of CD8 + resident memory T cells in lung mucosa after vaccination, resulting in the control of tumor growth. This work reinforces and explains why the intranasal route of vaccination is the most appropriate strategy for inducing these cells in the head and neck and pulmonary mucosa, which remains a major objective to overcome resistance to anti-PD-1/PD-L1, especially in cold tumors., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2021
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14. [NKT cells in the liver environment interact with Wnt/β-catenin and promote the emergence of liver carcinoma].

Author

Anson M, Viguier M, Perret C, and Couty JP

Subjects
Animals, Carcinoma genetics, Carcinoma immunology, Carcinoma metabolism, Cell Communication genetics, Cell Communication physiology, Cell Transformation, Neoplastic genetics, Cell Transformation, Neoplastic immunology, Cell Transformation, Neoplastic metabolism, Cellular Microenvironment genetics, Cellular Microenvironment immunology, Humans, Killer Cells, Natural metabolism, Liver cytology, Liver metabolism, Liver Neoplasms genetics, Liver Neoplasms immunology, Liver Neoplasms metabolism, Mice, Models, Biological, Signal Transduction genetics, Signal Transduction immunology, Signal Transduction physiology, Wnt Proteins genetics, Wnt Proteins physiology, beta Catenin genetics, beta Catenin physiology, Carcinoma etiology, Cellular Microenvironment physiology, Killer Cells, Natural physiology, Liver immunology, Liver Neoplasms etiology, Wnt Proteins metabolism, beta Catenin metabolism
Published
2012
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