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1. Bystander immunotherapy as a strategy to control allergen-driven airway inflammation

Author

Sébastien Fleury, Severine Navarro, Nicolas Glaichenhaus, A Kanda, David Dombrowicz, Anne Lazzari, Valérie Julia, Immunologie des muqueuses et inflammation, Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), Institut de pharmacologie moléculaire et cellulaire (IPMC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 (RNMCD), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Institut National de la Santé et de la Recherche Médicale (INSERM), This work was supported by a grant from the Fondation pour la Recherche Médicale and INSERM. S.N. was supported by a fellowship from the FRM, A.L. was supported by a fellowship from Vaincre la Mucoviscidose, and A.K is supported by a grant from the Agence Nationale de la Recherche (ANR)., We thank Nicolas Guy and the animal facility staff for their excellent animal care, as well as Julie Cazareth for the cell sorting experiments., Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), and Derudas, Marie-Hélène

Subjects
immune tolerance, T reg, medicine.medical_treatment, Protozoan Proteins, MESH: Ovalbumin/administration & dosage, MESH: Asthma/immunology, airway inflammation, Lymphocyte Activation, medicine.disease_cause, Immunoglobulin E, T-Lymphocytes, Regulatory, Mice, Th2, 0302 clinical medicine, Allergen, MESH: Antigens, Protozoan/immunology, Immunology and Allergy, CTLA-4 Antigen, MESH: Animals, IL-2 receptor, Desensitization (medicine), MESH: Immunoglobulin E/immunology, MESH: Th2 Cells/metabolism, 0303 health sciences, MESH: T-Lymphocytes, Regulatory/immunology, biology, respiratory system, MESH: Ovalbumin/immunology, MESH: Respiratory Hypersensitivity/metabolism, MESH: CTLA-4 Antigen/metabolism, 3. Good health, MESH: T-Lymphocytes, Regulatory/metabolism, [SDV.IMM]Life Sciences [q-bio]/Immunology, Bronchoalveolar Lavage Fluid, specific immunotherapy, MESH: Respiratory Hypersensitivity/immunology, MESH: Desensitization, Immunologic*/methods, [SDV.IMM] Life Sciences [q-bio]/Immunology, Ovalbumin, MESH: Mice, Transgenic, Immunology, MESH: Asthma/metabolism, Antigens, Protozoan, Mice, Transgenic, Article, Inducible T-Cell Co-Stimulator Protein, 03 medical and health sciences, Th2 Cells, MESH: Inducible T-Cell Co-Stimulator Protein/metabolism, Antigen, In vivo, MESH: Allergens/administration & dosage, Respiratory Hypersensitivity, medicine, Animals, MESH: Mice, 030304 developmental biology, business.industry, MESH: Interleukin-2 Receptor alpha Subunit/metabolism, Interleukin-2 Receptor alpha Subunit, Immunotherapy, Allergens, asthma, MESH: Protozoan Proteins/immunology, MESH: Lymphocyte Activation/immunology, MESH: Th2 Cells/immunology, respiratory tract diseases, MESH: Respiratory Hypersensitivity/therapy, Disease Models, Animal, Desensitization, Immunologic, MESH: Bronchoalveolar Lavage Fluid/immunology, biology.protein, MESH: Allergens/immunology, MESH: Disease Models, Animal, business, MESH: Asthma/therapy, 030215 immunology
Abstract

International audience; Allergic asthma is a chronic inflammatory disease characterized by airway hyperresponsiveness (AHR), lung infiltration of Th2 cells, and high levels of IgE. To date, allergen-specific immunotherapy (SIT) is the only treatment that effectively alleviates clinical symptoms and has a long-term effect after termination. Unfortunately, SIT is unsuitable for plurisensitized patients, and highly immunogenic allergens cannot be used. To overcome these hurdles, we sought to induce regulatory CD4(+) T cells (Treg) specific to an exogenous antigen that could be later activated as needed in vivo to control allergic responses. We have established an experimental approach in which mice tolerized to ovalbumin (OVA) were sensitized to the Leishmania homolog of receptors for activated c kinase (LACK) antigen, and subsequently challenged with aerosols of LACK alone or LACK and OVA together. Upon OVA administration, AHR and allergic airway responses were strongly reduced. OVA-induced suppression was mediated by CD25(+) Treg, required CTLA-4 and ICOS signaling and resulted in decreased numbers of migrating airway dendritic cells leading to a strong impairment in the proliferation of allergen-specific Th2 cells. Therefore, inducing Treg specific to a therapeutic antigen that could be further activated in vivo may represent a safe and novel curative approach for allergic asthma.Mucosal

Published
2015
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2. How to: Measuring blood cytokines in biological psychiatry using commercially available multiplex immunoassays

Author

Xavier Zendjidjian, Tifenn Le Carpentier, El Chérif Ibrahim, Anne Lazzari, Philippe Courtet, Mocrane Abbar, Jean Naudin, José Boucraut, Pierre Gressens, Nicolas Glaichenhaus, Marie-Noëlle Lefebvre, Raoul Belzeaux, Julia-Lou Consoloni, Département Universitaire de Psychiatrie - [Hôpital Sainte Marguerite - APHM] (Hôpitaux Sud), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud ), Fondation FondaMental [Créteil], Centre de recherche en neurobiologie - neurophysiologie de Marseille (CRN2M), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), CIC-CPCET, Hôpital de la Timone [CHU - APHM] (TIMONE), Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Immunologie des muqueuses et inflammation, COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), Neuroprotection du Cerveau en Développement / Promoting Research Oriented Towards Early Cns Therapies (PROTECT), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance Publique - Hôpitaux de Marseille (APHM), Service de psychiatrie adulte, Centre Hospitalier Universitaire de Nîmes (CHU Nîmes)-Hôpital Universitaire Carémeau [Nîmes] (CHU Nîmes), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Département des Urgences et Post-Urgences Psychiatriques, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Laboratoire d'Immunologie [Hôpital de la Conception - APHM], Assistance Publique - Hôpitaux de Marseille (APHM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital de la Conception [CHU - APHM] (LA CONCEPTION)-Centre National de la Recherche Scientifique (CNRS), ANR-13-SAMA-0002,VASPAC,Validation du concept spadine pour le traitement de la dépression(2013), ANR-11-LABX-0028,SIGNALIFE,Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie(2011), Ibrahim, El Chérif, Santé Mentale et Addictions - Validation du concept spadine pour le traitement de la dépression - - VASPAC2013 - ANR-13-SAMA-0002 - SAMENTA - VALID, Centres d'excellences - Réseau d'Innovation sur les Voies de Signalisation en Sciences de la Vie - - SIGNALIFE2011 - ANR-11-LABX-0028 - LABX - VALID, Hôpital Sainte-Marguerite [CHU - APHM] (Hôpitaux Sud )-Assistance Publique - Hôpitaux de Marseille (APHM)-Aix Marseille Université (AMU), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Université Nice Sophia Antipolis (... - 2019) (UNS), Hôpital Universitaire Carémeau [Nîmes] (CHU Nîmes), and Centre Hospitalier Universitaire de Nîmes (CHU Nîmes)-Centre Hospitalier Universitaire de Nîmes (CHU Nîmes)

Subjects
0301 basic medicine, Adult, Analyte, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, [SDV.MHEP.PSM] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health, Multiplex immunoassay, Inflammation, Disease, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Immune system, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Medicine, Humans, Multiplex, Biomarker discovery, Cytokine, Biological Psychiatry, Immunoassay, Psychiatry, Depressive Disorder, Major, Endocrine and Autonomic Systems, business.industry, Gold standard (test), 3. Good health, Psychiatry and Mental health, 030104 developmental biology, [SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health, Immunology, Cytokines, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Reagent Kits, Diagnostic, medicine.symptom, business, 030217 neurology & neurosurgery
Abstract

International audience; Cytokines produced by both immune and non-immune cells are likely to play roles in the development and/or progression of psychiatric disorders. Indeed, many investigators have compared the blood cytokine levels in psychiatric patients with those of healthy controls or monitored their levels in patients during disease progression to identify biomarkers. Nevertheless, very few studies have confirmed that such cytokines remain stable in healthy individuals through periods of weeks and months. This is an important issue to consider before using blood cytokine levels as biomarkers of disease traits, disease state, or treatment response. Although multiplex assay technology represents an advance in identifying biomarkers because it allows simultaneous examination of large panels of analytes from a small volume of sample, it is necessary to verify whether these assays yield enough sensitivity and reproducibility when applied to the blood from neuropsychiatric patients. Therefore, we compared two multiplex immunoassays, the bead-based Luminex® (Bio-Rad) and the electro-chemiluminescence-based V-plex® (MesoScaleDiscovery), for the detection and quantification of 31 cytokines, chemokines and growth factors in both the sera and plasma of patients with major depressive episodes (MDE) and age-and sex-matched healthy control subjects during a 30-week period. Although both platforms exhibited low coefficients of variability (CV) between the duplicates in the calibration curves, the linearity was better in general for the V-PLEX® platform. However, neither platform was able to detect the absolute values for all of the tested analytes. Among the 16 analytes that were detected by both assays, the intra-assay reproducibility was in general better with the V-PLEX® platform. Although it is not a general rule that the results from sera and plasma will be correlated, consistent results were more frequent with the V-PLEX® platform. Furthermore, the V-PLEX® results were more consistent with the gold standard ELISA simplex assay for IL-6 in both sera and plasma. The intra-individual variability of the measurements, among the sera and plasma for the 4 samples harvested from each healthy individual, was low for Eotaxin, G-CSF, IL-4, IL-7, IL-9, IL-12p40, IL-12p70, IL-15, MIP-1β, PDGF-BB, TNF, TNF-β and VEGF, but intermediate or high for IFN-γ, IL-6, IL-8, IL-10, and IP10. Together, these data suggest that extreme caution is needed in translating the results of multiplex cytokine profiling into biomarker discovery in psychiatry.

Published
2017
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3. Splenic CD8α+ dendritic cells undergo rapid programming by cytosolic bacteria and inflammation to induce protective CD8+ T-cell memory

Author

Saidi M.Homa Soudja, Grégoire Lauvau, Laura Campisi, Nicolas Glaichenhaus, Frédéric Brau, Anne Lazzari, Frederic Geissmann, Emilie Narni-Mancinelli, Julie Cazareth, Delphine Bassand, Immunologie des maladies infectieuses allergiques et autoimmunes, Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), Centre for Cellular and Molecular Biology of Inflammation, King‘s College London, Institut de pharmacologie moléculaire et cellulaire (IPMC), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Department of Microbiology and Immunology, and Albert Einstein College of Medicine [New York]

Subjects
MESH: Inflammation, Adoptive cell transfer, MESH: Spleen, Priming (immunology), Cell Count, MESH: T-Lymphocyte Subsets, MESH: Virulence, CD8-Positive T-Lymphocytes, MESH: Listeria monocytogenes, Lymphocyte Activation, MESH: Membrane Transport Proteins, Mice, Cytosol, 0302 clinical medicine, MESH: Cytosol, T-Lymphocyte Subsets, Immunology and Allergy, Cytotoxic T cell, MESH: Animals, Listeriosis, MESH: Bacterial Proteins, Cells, Cultured, Sequence Deletion, Adenosine Triphosphatases, Mice, Inbred BALB C, 0303 health sciences, MESH: Dendritic Cells, Virulence, biology, MESH: Sequence Deletion, Acquired immune system, MESH: CD8-Positive T-Lymphocytes, Adoptive Transfer, 3. Good health, MESH: Immunologic Memory, [SDV.IMM]Life Sciences [q-bio]/Immunology, medicine.symptom, MESH: Cells, Cultured, CD8 Antigens, Immunology, MESH: Mice, Inbred BALB C, Inflammation, 03 medical and health sciences, Bacterial Proteins, Antigen, MHC class I, MESH: Adenosine Triphosphatases, medicine, Animals, MESH: Lymphocyte Activation, MESH: Mice, 030304 developmental biology, SecA Proteins, MESH: Cell Count, Membrane Transport Proteins, Dendritic Cells, Listeria monocytogenes, MESH: Adoptive Transfer, MESH: Listeriosis, biology.protein, MESH: Antigens, CD8, Immunologic Memory, SEC Translocation Channels, Spleen, CD8, 030215 immunology
Abstract

International audience; Memory CD8(+) T lymphocytes are critical effector cells of the adaptive immune system mediating long-lived pathogen-specific protective immunity. Three signals - antigen, costimulation and inflammation - orchestrate optimal CD8(+) T-cell priming and differentiation into effector and memory cells and shape T-cell functional fate and ability to protect against challenge infections. While among the conventional spleen DCs (cDCs), the CD8α(+) but not the CD8α(-) cDCs most efficiently mediate CD8(+) T-cell priming, it is unclear which subset, irrespective of their capacity to process MHC class I-associated antigens, is most efficient at inducing naïve CD8(+) T-cell differentiation into pathogen-specific protective memory cells in vivo. Moreover, the origin of the required signals is still unclear. Using mice infected with the intracellular bacterium Listeria monocytogenes, we show that splenic CD8α(+) cDCs become endowed with all functional features to optimally prime protective memory CD8(+) T cells in vivo within only a few hours post-immunization. Such programming requires both cytosolic signals resulting from bacterial invasion of the host cells and extracellular inflammatory mediators. Thus, these data designate these cells as the best candidates to facilitate the development of cell-based vaccine therapy.

Published
2011
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4. CX3CL1 (fractalkine) and its receptor CX3CR1 regulate atopic dermatitis by controlling effector T cell retention in inflamed skin

Author

Valérie Julia, Julien Wartelle, Davide Pennino, Akira Kanda, Janne Prawitt, Delphine Staumont-Sallé, Cyrille Mionnet, Sébastien Fleury, Céline Lavogiez, David Dombrowicz, Nicolas Hornez, Olivier Molendi-Coste, Anne Lazzari, Emmanuel Bouchaert, Nicolas Glaichenhaus, Bart Staels, Anissa Fries, Emmanuel Delaporte, Centre d'Immunologie de Marseille - Luminy (CIML), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), and Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
0303 health sciences, Chemokine, Adoptive cell transfer, biology, T cell, [SDV]Life Sciences [q-bio], Immunology, medicine.disease, 3. Good health, 03 medical and health sciences, Chemokine receptor, 0302 clinical medicine, medicine.anatomical_structure, Immune system, Psoriasis, CX3CR1, medicine, biology.protein, Immunology and Allergy, CX3CL1, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 030215 immunology
Abstract

Atopic dermatitis (AD) is a chronic allergic dermatosis characterized by epidermal thickening and dermal inflammatory infiltrates with a dominant Th2 profile during the acute phase, whereas a Th1 profile is characteristic of the chronic stage. Among chemokines and chemokine receptors associated with inflammation, increased levels of CX(3)CL1 (fractalkine) and its unique receptor, CX(3)CR1, have been observed in human AD. We have thus investigated their role and mechanism of action in experimental models of AD and psoriasis. AD pathology and immune responses, but not psoriasis, were profoundly decreased in CX(3)CR1 deficient mice and upon blocking CX(3)CL1-CX(3)CR1 interactions in wild- type mice. CX(3)CR1 deficiency affected neither antigen presentation nor T cell proliferation in vivo upon skin sensitization, but CX(3)CR1 expression by both Th2 and Th1 cells was required to induce AD. Surprisingly, unlike in allergic asthma, where CX(3)CL1 and CX(3)CR1 regulate the pathology by controlling effector CD4(+) T cell survival within inflamed tissues, adoptive transfer experiments established CX(3)CR1 as a key regulator of CD4+ T cell retention in inflamed skin, indicating a new function for this chemokine receptor. Therefore, although CX(3)CR1 and CX3CL1 act through distinct mechanisms in different pathologies, our results further indicate their interest as promising therapeutic targets in allergic diseases.

Published
2014
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5. Induction of lectin-like transcript 1 (LLT1) protein cell surface expression by pathogens and interferon-γ contributes to modulate immune responses

Author

Anne Lazzari, Anne Neisig, Tao Dong, Katarina Håkansson, Veronique M. Braud, Elizabeth D. Galsgaard, Claire Germain, Gwénola Poupon, Perrine Knapnougel, Anders Meier, Nicolai Wagtmann, Teis Jensen, Pieter Spee, Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Biopharmaceuticals Research Unit (Novo Nordisk,), Novo Nordisk, Medical Research Council Human Immunology Unit, and University of Oxford [Oxford]- John Radcliffe Hospital [Oxford University Hospital]

Subjects
T-Lymphocytes, Biochemistry, MESH: Hematopoietic Stem Cells, Interleukin 21, Mice, 0302 clinical medicine, Cytotoxic T cell, MESH: Animals, MESH: Interferons, IL-2 receptor, CellPathogen-associated Molecular Pattern (PAMP), MESH: Receptors, Cell Surface, 0303 health sciences, Natural Killer (NK), Toll-Like Receptors, Natural killer T cell, MESH: Gene Expression Regulation, 3. Good health, Cell biology, MESH: Leukocytes, Mononuclear, MESH: NK Cell Lectin-Like Receptor Subfamily B, medicine.anatomical_structure, Interleukin 12, Interferon, [SDV.IMM]Life Sciences [q-bio]/Immunology, Toll-like Receptor (TLR), MESH: Toll-Like Receptors, NK Cell Lectin-Like Receptor Subfamily B, NK T cell proliferation, MESH: Interferon-gamma, T cell, T Cell, Immunology, Receptors, Cell Surface, Biology, Models, Biological, Cell Line, 03 medical and health sciences, Interferon-gamma, LLT1, medicine, Animals, Humans, Lectins, C-Type, Antigen-presenting cell, Molecular Biology, MESH: Mice, 030304 developmental biology, MESH: Humans, MESH: Immune System, Cell Membrane, MESH: Models, Biological, Cell Biology, Hematopoietic Stem Cells, Molecular biology, MESH: Cell Line, MESH: T-Lymphocytes, Gene Expression Regulation, Immune System, Leukocytes, Mononuclear, Interferons, MESH: Lectins, C-Type, 030215 immunology, CD161, MESH: Cell Membrane
Abstract

International audience; CD161 is a C-type lectin-like receptor expressed on human natural killer (NK) cells and subsets of T cells. CD161 has been described as an inhibitory receptor that regulates NK cell-mediated cytotoxicity and IFN-γ production. Its role on T cells has remained unclear. Studies have shown that triggering of CD161 enhances NK T cell proliferation and T cell-IFN-γ production while inhibiting TNF-α production by CD8(+) T cells. Lectin-like transcript 1 (LLT1), the ligand of CD161, was found to be expressed on Toll-like receptor (TLR)-activated plasmacytoid and monocyte-derived dendritic cells (DC) and on activated B cells. Using newly developed anti-LLT1 mAbs, we show that LLT1 is not expressed on the surface of circulating B and T lymphocytes, NK cells, monocytes, and dendritic cells but that LLT1 is up-regulated upon activation. Not only TLR-stimulated dendritic cells and B cells but also T cell receptor-activated T cells and activated NK cells up-regulate LLT1. Interestingly, IFN-γ increases LLT1 expression level on antigen-presenting cells. LLT1 is also induced on B cells upon viral infection such as Epstein-Barr virus or HIV infection and in inflamed tonsils. Finally, expression of LLT1 on B cells inhibits NK cell function but costimulates T cell proliferation or IFN-γ production, and coengagement of CD161 with CD3 increases IL-17 secretion. Altogether, our results point toward a role for LLT1/CD161 in modulating immune responses to pathogens.

Published
2011
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6. Langerin+ dendritic cells are responsible for LPS-induced reactivation of allergen-specific Th2 responses in postasthmatic mice

Author

Julie Cazareth, A Ortiz-Stern, Valérie Julia, David Dombrowicz, Akira Kanda, Anne Lazzari, Nicolas Glaichenhaus, Cyrille Mionnet, Sébastien Fleury, Centre d'Immunologie de Marseille - Luminy (CIML), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Aix Marseille Université (AMU), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA), Immunologie des maladies infectieuses allergiques et autoimmunes, COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP), Université Lille Nord de France (COMUE), Institut de pharmacologie moléculaire et cellulaire (IPMC), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), and Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Lipopolysaccharides, Lipopolysaccharide, MESH: Asthma, Receptors, Antigen, T-Cell, alpha-beta, [SDV]Life Sciences [q-bio], Lymphocyte Activation, medicine.disease_cause, Mice, chemistry.chemical_compound, 0302 clinical medicine, Allergen, Cell Movement, Immunology and Allergy, MESH: Animals, Receptor, Lung, MESH: Cell Movement, Cells, Cultured, ComputingMilieux_MISCELLANEOUS, Mice, Inbred BALB C, 0303 health sciences, MESH: Receptors, Antigen, T-Cell, alpha-beta, biology, integumentary system, MESH: Dendritic Cells, respiratory system, 3. Good health, medicine.anatomical_structure, Antigens, Surface, [SDV.IMM]Life Sciences [q-bio]/Immunology, MESH: Cells, Cultured, MESH: Allergens, Langerin, Ovalbumin, MESH: Mice, Transgenic, MESH: Antigens, Surface, T cell, Immunology, MESH: Mice, Inbred BALB C, Mice, Transgenic, 03 medical and health sciences, Th2 Cells, Antigen, MESH: Eosinophils, MESH: Th2 Cells, MESH: Mannose-Binding Lectins, medicine, Animals, Humans, Lectins, C-Type, MESH: Lung, MESH: Lymphocyte Activation, MESH: Mice, 030304 developmental biology, MESH: Ovalbumin, MESH: Humans, Dendritic Cells, Allergens, Eosinophil, Asthma, respiratory tract diseases, Eosinophils, Mannose-Binding Lectins, chemistry, biology.protein, MESH: Lipopolysaccharides, MESH: Lectins, C-Type, 030215 immunology
Abstract

International audience; Allergic asthma is a T cell-dependent inflammatory lung disease that results from complex interactions between genetic predisposition and environmental factors, including exposure to lipopolysaccharide (LPS). In this study, we have shown that airway LPS exposure was sufficient to induce airway hyperreactivity (AHR) and eosinophil recruitment in mice that had previously experienced an acute episode of allergic asthma. LPS-induced disease reactivation depended on the activation of allergen-specific CD4(+) T cells by a subset of lung langerin(+) dendritic cells (DCs) that retained the allergen. Upon LPS exposure, migration of langerin(+) DCs from lungs to draining lymph nodes increased and LPS-exposed langerin(+) DCs instructed CD4(+) T cells toward a T helper (Th) 2 response. Selective depletion of langerin(+) DCs prevented LPS-induced eosinophil recruitment and T-cell activation, further demonstrating a critical role for langerin(+) DCs in disease reactivation. This finding provides a possible explanation for the subclinical worsening of asthmatics following exposure to low-dose LPS.

Published
2011
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7. The oral administration of bacterial extracts prevents asthma via the recruitment of regulatory T cells to the airways

Author

Valérie Julia, Tim Sparwasser, Anne Lazzari, C Chiavaroli, Akira Kanda, Nicolas Glaichenhaus, Severine Navarro, G Cossalter, David Dombrowicz, Julie Cazareth, Sébastien Fleury, Immunologie des maladies infectieuses allergiques et autoimmunes, Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Thoiry, Inconnu, Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP), Université Lille Nord de France (COMUE), Institut de pharmacologie moléculaire et cellulaire (IPMC), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS), Institute of Infection Immunology (TWINCORE), Center for Experimental and Clinical Infection Research, and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)

Subjects
CD4-Positive T-Lymphocytes, Adoptive cell transfer, MESH: Interleukin-10, MESH: Asthma, Respiratory System, Administration, Oral, T-Lymphocytes, Regulatory, Mice, 0302 clinical medicine, Oral administration, MESH: Cell Extracts, Immunology and Allergy, MESH: Animals, MESH: Respiratory System, MESH: Cytokines, 0303 health sciences, Mice, Inbred BALB C, Respiratory tract infections, MESH: CD4-Positive T-Lymphocytes, FOXP3, Forkhead Transcription Factors, Adoptive Transfer, 3. Good health, Interleukin-10, MESH: Administration, Oral, [SDV.IMM]Life Sciences [q-bio]/Immunology, Cytokines, MESH: Myeloid Differentiation Factor 88, Oral treatment, Immunology, MESH: Mice, Inbred BALB C, 03 medical and health sciences, MESH: Forkhead Transcription Factors, medicine, Animals, MESH: Mice, Gene, 030304 developmental biology, Asthma, Bacteria, business.industry, MESH: T-Lymphocytes, Regulatory, medicine.disease, MESH: Adoptive Transfer, MESH: Bacteria, Myeloid Differentiation Factor 88, Airway, business, 030215 immunology
Abstract

International audience; The prevalence of asthma has steadily increased during the last decade, probably as the result of changes in the environment, including reduced microbial exposure during infancy. Accordingly, experimental studies have shown that deliberate infections with live pathogens prevent the development of allergic airway diseases in mice. Bacterial extracts are currently used in children suffering from repeated upper respiratory tract infections. In the present study, we have investigated whether bacterial extracts, commercially available as Broncho-Vaxom (BV), could prevent allergic airway disease in mice. Oral treatment with BV suppressed airway inflammation through interleukin-10 (IL-10)-dependent and MyD88 (myeloid differentiation primary response gene (88))-dependent mechanisms and induced the conversion of FoxP3 (forkhead box P3)(-) T cells into FoxP3(+) regulatory T cells. Furthermore, CD4(+) T cells purified from the trachea of BV-treated mice conferred protection against airway inflammation when adoptively transferred into sensitized mice. Therefore, treatment with BV could possibly be a safe and efficient strategy to prevent the development of allergic diseases in children.

Published
2010
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8. Lectin-like transcript 1 is a marker of germinal center-derived B-cell non-Hodgkin's lymphomas dampening natural killer cell functions

Author

Karin Tarte, Catherine Hervouet, Luc Xerri, Anne Lazzari, Franck Bihl, Claire Germain, Nedra Tekaya, Elisabeth D. Galsgaard, Patrick Tas, Pieter Spee, Anne-Sophie Gallouet, Céline Pangault, Fabienne Anjuère, Julien Fassy, Gwénola Poupon, Thierry Guillaudeux, Veronique M. Braud, Institut de pharmacologie moléculaire et cellulaire (IPMC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Microenvironnement et cancer (MiCa), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Etablissement Français du Sang Bretagne, EFS, Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Novo Nordisk Foundation Center for Biosustainability, Technical University of Denmark [Lyngby] (DTU), CHU Pontchaillou [Rennes], Centre de Recherche en Cancérologie de Marseille (CRCM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Université Nice Sophia Antipolis (... - 2019) (UNS), Université Côte d'Azur (UCA)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), Université de Rennes (UNIV-RENNES), Novo Nordisk A/S [Maløv, Denmark], Biopharmaceuticals Research Unit (Novo Nordisk,), Novo Nordisk, Service de Biologie, CRLCC Eugène Marquis (CRLCC), Département de Biopathologie, Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Danmarks Tekniske Universitet = Technical University of Denmark (DTU), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, and Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV]Life Sciences [q-bio], Immunology, Follicular lymphoma, Biology, Natural killer cell, 03 medical and health sciences, 0302 clinical medicine, LLT1, immune system diseases, hemic and lymphatic diseases, medicine, Immunology and Allergy, non-Hodgkin's B-cell lymphoma, Receptor, B cell, Original Research, 030304 developmental biology, 0303 health sciences, natural killer cells, Germinal center, medicine.disease, 3. Good health, Lymphoma, medicine.anatomical_structure, Oncology, germinal center, Biomarker (medicine), Lymph, CD161, 030215 immunology
Abstract

International audience; Non-Hodgkin's lymphomas (NHLs) are malignant neoplasms which are clinically and biologically diverse. Their incidence is constantly increasing and despite treatment advances, there is a need for novel targeted therapies. Here, we identified Lectin-like transcript 1 (LLT1) as a biomarker of germinal center (GC)-derived B-cell NHLs. LLT1 identifies GC B cells in reactive tonsils and lymph nodes and its expression is maintained in B-cell NHLs which derive from GC, including Burkitt lymphoma (BL), follicular lymphoma (FL), and GC-derived diffuse large B-cell lymphoma (DLBCL). We further show that LLT1 expression by tumors dampens natural killer (NK) cell functions following interaction with its receptor CD161, uncovering a potential immune escape mechanism. Our results pinpoint LLT1 as a novel biomarker of GC-derived B-cell NHLs and as a candidate target for innovative immunotherapies

Published
2015
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