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4 results on '"Peggy Kirstetter"'

1. Dendritic Cells Require TMEM176A/B Ion Channels for Optimal MHC Class II Antigen Presentation to Naive CD4 + T Cells

Author

Saeed Abdu Rahiman, Melanie Lancien, Amandine Even, Séverine Remy, Maria-Cristina Cuturi, Veronica De Simone, Lucile Gueno, Elise Chiffoleau, Sonia Salle, Aurélie Moreau, Geraldine Bienvenu, Steven M. Kerfoot, Alice Molle, Gaelle Beriou, Flora Coulon, Régis Josien, Magalie Feyeux, Franck Perez, Susan Chan, Cynthia Fourgeux, Emmanuel Merieau, Gianluca Matteoli, Peggy Kirstetter, Laurence Bouchet-Delbos, Jeremie Poschmann, Cédric Louvet, Gaelle Boncompain, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Centre hospitalier universitaire de Nantes (CHU Nantes), Structure fédérative de recherche François Bonamy (SFR François Bonamy), Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche en Santé de l'Université de Nantes (IRS-UN), University of Western Ontario (UWO), Catholic University of Leuven - Katholieke Universiteit Leuven (KU Leuven), Biologie Cellulaire et Cancer, Institut Curie [Paris]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), and Boncompain, Gaelle

Subjects
CD4-Positive T-Lymphocytes, Male, [SDV.IMM] Life Sciences [q-bio]/Immunology, T cell, [SDV]Life Sciences [q-bio], Genes, MHC Class II, Immunology, Golgi Apparatus, Priming (immunology), Tretinoin, Endosomes, Ion Channels, MHC class II antigen, Mice, 03 medical and health sciences, 0302 clinical medicine, Intestinal mucosa, medicine, Animals, Immunology and Allergy, Lymphocytes, Intestinal Mucosa, Ion channel, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, Mice, Knockout, Orphan receptor, Antigen Presentation, 0303 health sciences, MHC class II, biology, Chemistry, Innate lymphoid cell, Histocompatibility Antigens Class II, Membrane Proteins, Dendritic Cells, Immunity, Innate, Cell biology, Mice, Inbred C57BL, medicine.anatomical_structure, 030220 oncology & carcinogenesis, biology.protein, Th17 Cells, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Lysosomes
Abstract

Intracellular ion fluxes emerge as critical actors of immunoregulation but still remain poorly explored. In this study, we investigated the role of the redundant cation channels TMEM176A and TMEM176B (TMEM176A/B) in retinoic acid–related orphan receptor γt+ cells and conventional dendritic cells (DCs) using germline and conditional double knockout mice. Although Tmem176a/b appeared surprisingly dispensable for the protective function of Th17 and group 3 innate lymphoid cells in the intestinal mucosa, we found that they were required in conventional DCs for optimal Ag processing and presentation to CD4+ T cells. Using a real-time imaging method, we show that TMEM176A/B accumulate in dynamic post-Golgi vesicles preferentially linked to the late endolysosomal system and strongly colocalize with HLA-DM. Taken together, our results suggest that TMEM176A/B ion channels play a direct role in the MHC class II compartment of DCs for the fine regulation of Ag presentation and naive CD4+ T cell priming.

Published
2021

2. Dendritic cells require TMEM176A/B ion channels for optimal MHC II antigen presentation to naive CD4 + T cells

Author

Peggy Kirstetter, Gianluca Matteoli, Emmanuel Merieau, Gaelle Beriou, Saeed Abdu Rahiman, Sonia Salle, Franck Perez, Lucile Gueno, Flora Coulon, Laurence Bouchet-Delbos, Maria-Cristina Cuturi, Cédric Louvet, Jeremie Poschmann, Aurélie Moreau, Geraldine Bienvenu, Steven M. Kerfoot, Alice Molle, Régis Josien, Elise Chiffoleau, Melanie Lancien, Séverine Remy, Amandine Even, Gaelle Boncompain, Susan Chan, Cynthia Fourgeux, Veronica De Simone, Institut Curie [Paris], Biologie Cellulaire et Cancer, Institut Curie [Paris]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Université de Nantes (UN), and Centre hospitalier universitaire de Nantes (CHU Nantes)

Subjects
0303 health sciences, Chemistry, Antigen processing, T cell, [SDV]Life Sciences [q-bio], Innate lymphoid cell, Antigen presentation, Priming (immunology), Cell biology, 03 medical and health sciences, 0302 clinical medicine, medicine.anatomical_structure, Intestinal mucosa, 030220 oncology & carcinogenesis, medicine, Intracellular, Ion channel, 030304 developmental biology
Abstract

SummaryIntracellular ion fluxes emerge as critical actors of immunoregulation but still remain poorly explored. Here we investigated the role of the redundant cation channels TMEM176A and TMEM176B (TMEM176A/B) in RORγt+ cells and conventional dendritic cells (cDCs) using germline and conditional double knock-out (DKO) mice. While Tmem176a/b appeared surprisingly dispensable for the protective function of Th17 and group 3 innate lymphoid cells (ILC3s) in the intestinal mucosa, we found that they were required in cDCs for optimal antigen processing and presentation to CD4+ T cells. Using a real-time imaging method, we show that TMEM176A/B accumulate in dynamic post-Golgi vesicles preferentially linked to the late endolysosomal system and strongly colocalize with HLA-DM. Together, our results suggest that TMEM176A/B ion channels play a direct role in the MHC II compartment (MIIC) of DCs for the fine regulation of antigen presentation and naive CD4+ T cell priming.

Published
2020

3. Treatment of MCPT8 DTR mice with high- or low-dose diphtheria toxin leads to differential depletion of basophils and granulocyte-macrophage progenitors

Author

Jiagui Li, Mei Li, Peggy Kirstetter, Susan Chan, Carole El Hachem, Pierre Hener, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Louis Pasteur - Strasbourg I, and kirstetter, peggy

Subjects
0301 basic medicine, Allergy, Neutrophils, [SDV]Life Sciences [q-bio], Immunology, chemical and pharmacologic phenomena, Granulocyte, Biology, 03 medical and health sciences, chemistry.chemical_compound, Immune system, In vivo, medicine, Immunology and Allergy, Macrophage, Fluorescein isothiocyanate, ComputingMilieux_MISCELLANEOUS, Diphtheria toxin, Allergic contact dermatitis (ACD), medicine.disease, 3. Good health, [SDV] Life Sciences [q-bio], Eosinophils, Haematopoiesis, 030104 developmental biology, medicine.anatomical_structure, chemistry, Diphtheria toxin receptor (DTR), [SDV.IMM]Life Sciences [q-bio]/Immunology, MCPT8
Abstract

International audience; Basophils have been recently recognized to play important roles in type 2 immune responses during allergies and parasitic infection, largely due to the development of novel tools for the in vivo study of these cells. As such, the genetically-engineered MCPT8DTR mouse line has been used to specifically deplete basophils following treatment with diphtheria toxin (DT). In this study, we showed that DT-injected MCPT8DTR mice exhibited a striking decrease of eosinophils and neutrophils in skin when subjected to a hapten fluorescein isothiocyanate (FITC)-induced allergic contact dermatitis (ACD) experimental protocol. Unexpectedly, we found that loss of skin eosinophils and neutrophils was not due to a lack of basophil-mediated recruitment, as DT injection caused a systemic reduction of eosinophils and neutrophils in MCPT8DTR mice in a time-dependent manner. Furthermore, we found that hematopoietic stem-cell-derived granulocyte-macrophage progenitors (GMPs) expressed MCPT8 gene, and that these cells were depleted upon DT injection. Finally, we optimized a protocol in which a low-dose DT achieved a better specificity for depleting basophils, but not GMPs, in MCPT8DTR mice, and demonstrate that basophils do not play a major role in recruiting eosinophils and neutrophils to ACD skin. These data provide new and valuable information about functional studies of basophils.

Published
2018

4. Therapeutical modulation of plasmacytoid dendritic cells in experimental arthritis

Author

Birgit Niederreiter, Jean Sibilia, Antonia Puchner, Gernot Schabbauer, Philippe Kastner, Thierry F. Vandamme, Seiamak Bahram, Christopher G. Mueller, Victoria Saferding, Vincent Flacher, Stephan Blüml, Martin Holcmann, Philippe Georgel, Benjamin Voisin, Peggy Kirstetter, Susan Chan, Ghada Alsaleh, Ramzi Nehmar, Alexandre Mariotte, Immuno-Rhumatologie Moléculaire, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Immunopathologie et chimie thérapeutique (ICT), Institut de biologie moléculaire et cellulaire (IBMC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Chimie des Systèmes Fonctionnels, Centre National de la Recherche Scientifique (CNRS), Conception et application de molécules bioactives (CAMB), Institut de Chimie du CNRS (INC)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Centre for Integrative Biology - CBI (Inserm U964 - CNRS UMR7104 - IGBMC), Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de génétique et biologie moléculaire et cellulaire (IGBMC), Université Louis Pasteur - Strasbourg I-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), univOAK, Archive ouverte, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg (UNISTRA), Centre de Recherche d’Immunologie et d’Hématologie [Strasbourg], Centre de recherche du médicament Medalis - Drug Discovery Center [LabEx], Medizinische Universität Wien = Medical University of Vienna, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)

Subjects
0301 basic medicine, rheumatoid arthritis, [SDV]Life Sciences [q-bio], medicine.medical_treatment, Arthritis, Imiquimod, Arthritis, Rheumatoid, Mice, 0302 clinical medicine, Interferon, Immunology and Allergy, Medicine, Mice, Knockout, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Membrane Glycoproteins, Reverse Transcriptase Polymerase Chain Reaction, hemic and immune systems, Flow Cytometry, 3. Good health, Cytokine, plasmacytoid dendritic cells, Rheumatoid arthritis, Interferon Type I, Aminoquinolines, Cytokines, Tumor necrosis factor alpha, medicine.symptom, medicine.drug, Immunology, Inflammation, Enzyme-Linked Immunosorbent Assay, Mice, Transgenic, Sciences du Vivant [q-bio]/Médecine humaine et pathologie, 03 medical and health sciences, Ikaros Transcription Factor, Rheumatology, Adjuvants, Immunologic, Animals, Humans, 030203 arthritis & rheumatology, business.industry, Tumor Necrosis Factor-alpha, Gene Expression Profiling, Dendritic Cells, medicine.disease, Arthritis, Experimental, imiquimod, Disease Models, Animal, 030104 developmental biology, Toll-Like Receptor 7, business, Interferon type I, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Objective: The role of plasmacytoid dendritic cells (PDCs) and type I interferons (IFNs) in rheumatoid arthritis (RA) remains a subject of controversy. This study was undertaken to explore the contribution of PDCs and type I IFNs to RA pathogenesis using various animal models of PDC depletion and to monitor the effect of localized PDC recruitment and activation on joint inflammation and bone damage.Methods: Mice with K/BxN serum-induced arthritis, collagen-induced arthritis, and human tumor necrosis factor transgene insertion were studied. Symptoms were evaluated by visual scoring, quantification of paw swelling, determination of cytokine levels by enzyme-linked immunosorbent assay, and histologic analysis. Imiquimod-dependent therapeutic effects were monitored by transcriptome analysis (using quantitative reverse transcriptase-polymerase chain reaction) and flow cytometric analysis of the periarticular tissue.Results: PDC-deficient mice showed exacerbation of inflammatory and arthritis symptoms after arthritogenic serum transfer. In contrast, enhancing PDC recruitment and activation to arthritic joints by topical application of the Toll-like receptor 7 (TLR-7) agonist imiquimod significantly ameliorated arthritis in various mouse models. Imiquimod induced an IFN signature and led to reduced infiltration of inflammatory cells.Conclusion: The therapeutic effects of imiquimod on joint inflammation and bone destruction are dependent on TLR-7 sensing by PDCs and type I IFN signaling. Our findings indicate that local recruitment and activation of PDCs represents an attractive therapeutic opportunity for RA patients.

Published
2017

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