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6 results on '"MESH: Leukocytes, Mononuclear/metabolism"'

1. Evaluation of anti-proliferative and anti-inflammatory activities of Pelagia noctiluca venom in Lipopolysaccharide/Interferon-γ stimulated RAW264.7 macrophages

Author

Rabiaa M. Sghaier, Yosra Ayed, Dhafer Laouini, Hassen Bacha, College of Dentistry, Taibah University, Laboratory for Research on Biologically Compatible Compounds, Faculty of Dental Medicine of Monastir, Laboratoire de Transmission, Contrôle et Immunobiologie des Infections ( LR11IPT02 ), Institut Pasteur de Tunis-Réseau International des Instituts Pasteur ( RIIP ), Université Tunis El Manar ( UTM ), Faculté de Médecine Dentaire de Monastir [Tunisie] (FMDM), Laboratoire de Transmission, Contrôle et Immunobiologie des Infections - Laboratory of Transmission, Control and Immunobiology of Infection (LR11IPT02), Institut Pasteur de Tunis, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Université de Tunis El Manar (UTM), and Université de Jendouba (UJ)

Subjects
Lipopolysaccharides, 0301 basic medicine, Lipopolysaccharide, MESH: Cell Survival/physiology, MESH: Lipopolysaccharides/toxicity, [SDV]Life Sciences [q-bio], Anti-Inflammatory Agents, Drug Evaluation, Preclinical, Nitric Oxide Synthase Type II, Venom, MESH: Cell Proliferation/drug effects, MESH: Leukocytes, Mononuclear/drug effects, MESH: Dose-Response Relationship, Drug, Mice, chemistry.chemical_compound, 0302 clinical medicine, MESH: Animals, MESH: Interferon-gamma/toxicity, MESH: Cnidarian Venoms/isolation & purification, Cell proliferation, ComputingMilieux_MISCELLANEOUS, MTT assay, biology, MESH: Nitric Oxide Synthase Type II/metabolism, General Medicine, [SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciences, 3. Good health, MESH: Drug Evaluation, Preclinical/methods, 030220 oncology & carcinogenesis, MESH: Leukocytes, Mononuclear/metabolism, Cell Survival, Peripheral blood mononuclear cell, MESH: Cnidarian Venoms/pharmacology, Cell Line, Nitric oxide, Microbiology, Interferon-gamma, 03 medical and health sciences, Anti-inflammatory activity, Cnidarian Venoms, Animals, Humans, MESH: Macrophages/metabolism, MESH: Nitric Oxide Synthase Type II/antagonists & inhibitors, MESH: Macrophages/drug effects, MESH: Mice, Pelagia noctiluca, Pharmacology, MESH: K562 Cells, MESH: Humans, Dose-Response Relationship, Drug, [ SDV ] Life Sciences [q-bio], Cell growth, Macrophages, MESH: Cell Proliferation/physiology, biology.organism_classification, MESH: Anti-Inflammatory Agents/isolation & purification, Molecular biology, MESH: Cell Line, 030104 developmental biology, chemistry, Cell culture, Leukocytes, Mononuclear, MESH: Anti-Inflammatory Agents/pharmacology, K562 Cells, MESH: Cell Survival/drug effects, K562 cells
Abstract

International audience; Components of Pelagia noctiluca (P. noctiluca) venom were evaluated for their anticancer and nitric Oxide (NO) inhibition activities. Three fractions, out of four, obtained by gel filtration on Sephadex G75 of P. noctiluca venom revealed an important selective anti-proliferative activity on several cell lines such as human bladder carcinoma (RT112), human glioblastoma (U87), and human myelogenous leukemia (K562) but not on mitogen-stimulated peripheral blood mononuclear cells. Interestingly, P. noctiluca components showed an important dose-dependent anti-inflammatory activity, through inhibition of NO production via transcriptional regulation of Inducible NO Synthase (iNOS), in IFN-γ/LPS stimulated RAW 264.7 macrophages. These data strongly suggest that P. noctiluca venom could be used as a natural inhibitor of cancer cell lines and a potent anti-inflammatory agent for the treatment of anti-inflammatory diseases.

Published
2016
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2. Soluble Siglec-5 associates to PSGL-1 and displays anti-inflammatory activity

Author

Pepin, Marion, Mezouar, Soraya, Pegon, Julie, Muczynski, Vincent, Adam, Frédéric, Bianchini, Elsa P, Bazaa, Amine, Proulle, Valerie, Rupin, Alain, Paysant, Jerome, Panicot-Dubois, Laurence, Christophe, Olivier D., Dubois, Christophe, Lenting, Peter J, Denis, Cécile V, Hémostase, Inflammation, Thrombose (HITH - U1176 Inserm - CHU Bicêtre), Université Paris-Sud - Paris 11 (UP11)-AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre)-Institut National de la Santé et de la Recherche Médicale (INSERM), Vascular research center of Marseille (VRCM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Aix Marseille Université (AMU), Service d'hématologie, immunologie biologiques et cytogénétique, Université Paris-Sud - Paris 11 (UP11)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Bicêtre, Institut de Recherches Internationales Servier [Suresnes] (IRIS), The study was financially supported by a PhD-research grant from Institut Servier & Association Nationale de la Recherche Technique (Contrat CIFRE) to JPe, and an Inserm-Poste d’Accueil-grant (# ASC13101LSA) to MP., Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), and Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
MESH: Anti-Inflammatory Agents/pharmacology, E-SELECTIN LIGAND-1, [SDV]Life Sciences [q-bio], Anti-Inflammatory Agents, MESH: Membrane Glycoproteins/genetics, MESH: Antigens, Differentiation, Myelomonocytic/metabolism, MESH: Lectins/metabolism, MESH: Antigens, CD/pharmacology, MESH: Leukocytes, Mononuclear/drug effects, Lectins, MESH: Animals, MYELOID CELLS, MESH: E-Selectin/metabolism, NEUTROPHILS, IN-VIVO, MESH: Inflammation/drug therapy, Membrane Glycoproteins, MESH: Inflammation/chemically induced, MESH: Inflammation/pathology, MESH: Membrane Glycoproteins/metabolism, MESH: Leukocyte Rolling/physiology, P-Selectin, Female, E-Selectin, MESH: Leukocytes, Mononuclear/metabolism, CD33-RELATED SIGLECS, VON-WILLEBRAND-FACTOR, MESH: Lectins/pharmacology, Antigens, Differentiation, Myelomonocytic, MESH: Antigens, Differentiation, Myelomonocytic/pharmacology, MESH: Tumor Necrosis Factor-alpha/toxicity, GLYCOPROTEIN LIGAND, MESH: Antigens, CD/metabolism, Article, MESH: Mice, Inbred C57BL, Antigens, CD, Animals, Humans, Leukocyte Rolling, Protein Interaction Domains and Motifs, MESH: Antigens, Differentiation, Myelomonocytic/genetics, SIALIC-ACID, Inflammation, MESH: Protein Interaction Domains and Motifs, MESH: Humans, Tumor Necrosis Factor-alpha, MESH: Lectins/genetics, MESH: Solubility, Mice, Inbred C57BL, Disease Models, Animal, Solubility, Leukocytes, Mononuclear, MESH: Antigens, CD/genetics, IMMUNE-SYSTEM, MESH: Disease Models, Animal, MESH: Female, MESH: P-Selectin/metabolism
Abstract

International audience; Interactions between endothelial selectins and the leukocyte counter-receptor PSGL1 mediates leukocyte recruitment to inflammation sites. PSGL1 is highly sialylated, making it a potential ligand for Siglec-5, a leukocyte-receptor that recognizes sialic acid structures. Binding assays using soluble Siglec-5 variants (sSiglec-5/C4BP and sSiglec-5/Fc) revealed a dose- and calcium-dependent binding to PSGL1. Pre-treatment of PSGL1 with sialidase reduced Siglec-5 binding by 79 ± 4%. In confocal immune-fluorescence assays, we observed that 50% of Peripheral Blood Mononuclear Cells (PBMCs) simultaneously express PSGL1 and Siglec-5. Duolink-proximity ligation analysis demonstrated that PSGL1 and Siglec-5 are in close proximity (

Published
2016
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3. Thrombospondin-1-derived peptide RFYVVMWK improves the adhesive phenotype of CD34sup+/sup cells from atherosclerotic patients with type 2 diabetes

Author

Cointe , Sylvie, Rhéaume , Éric, Martel , Catherine, Blanc-Brude , Olivier, Dubé , Evemie, Sabatier , Florence, DIGNAT-GEORGE , Françoise, Tardif , Jean-Claude, Bonnefoy , Arnaud, Vascular research center of Marseille (VRCM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Aix Marseille Université (AMU), Montreal Heart Institute - Institut de Cardiologie de Montréal, Université de Montréal (UdeM), Paris-Centre de Recherche Cardiovasculaire (PARCC - UMR-S 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)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), CHU Sainte Justine [Montréal], Hôpital de la Conception [CHU - APHM] (LA CONCEPTION), This work was supported in part by the Agence Nationale de la Recherche (Grant No. ANR-07-PHYSIO-025-02), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 (UPD5)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital de la Conception [CHU - APHM] (LA CONCEPTION ), Vascular research center of Marseille ( VRCM ), Aix Marseille Université ( AMU ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut de génétique et microbiologie [Orsay] ( IGM ), Université Paris-Sud - Paris 11 ( UP11 ) -Centre National de la Recherche Scientifique ( CNRS ), Paris-Centre de Recherche Cardiovasculaire ( PARCC - U970 ), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Institut Armand Frappier ( INRS-IAF ), Institut National de la Recherche Scientifique [Québec] ( INRS ) -Réseau International des Instituts Pasteur ( RIIP ) -Institut Armand Frappier, Hôpital de la Conception [CHU - APHM] ( LA CONCEPTION ), Département de géographie, Université du Québec à Montréal ( UQAM ), and Issekinicho Editions

Subjects
MESH: Angina, Stable/metabolism, MESH: Acute Coronary Syndrome/metabolism, MESH: Diabetes Mellitus, Type 2/immunology, [SDV]Life Sciences [q-bio], MESH: Collagen/metabolism, MESH: Diabetes Mellitus, Type 2/metabolism, MESH: Atherosclerosis/metabolism, MESH: Peptides/chemistry, MESH: Cell Adhesion/physiology, MESH: Leukocytes, Mononuclear/metabolism, MESH: Acute Coronary Syndrome/immunology, MESH: Atherosclerosis/immunology, MESH: Platelet Aggregation Inhibitors/chemistry, MESH: Human Umbilical Vein Endothelial Cells, Type 2 diabetes (T2D), CD47, MESH: Aged, MESH: Coronary Artery Disease/immunology, MESH: Humans, MESH: Middle Aged, [ SDV ] Life Sciences [q-bio], MESH: Platelet Aggregation Inhibitors/pharmacology, MESH: Peptides/pharmacology, Atherosclerosis, MESH: Male, MESH: Coronary Artery Disease/metabolism, MESH: Vitronectin/metabolism, MESH: Angina, Stable/immunology, Thrombospondin-1 (TSP-1), MESH: Thrombospondin 1/chemistry, MESH: Antigens, CD34/metabolism, CD34, MESH: Cells, Cultured
Abstract

International audience; Background: CD34(+) progenitor cells are growingly used for vascular repair. However, in diabetic individuals with cardiovascular diseases, these cells have dysfunctional engraftment capabilities, which compromise their use for autologous cell therapy. The thrombospondin-1-derived peptide RFYVVMWK has previously been reported to stimulate cell adhesiveness through CD47 and integrin activation pathways.Objectives: Our aim was to test whether RFYVVMWK preconditioning could modulate CD34(+) cells phenotype and enhance its pro-adhesive properties in diabetic patients.Patients/methods: Peripheral blood mononuclear CD34(+) cells isolated from 40 atherosclerotic patients with (T2D; n=20) or without (NonT2D; n=20) type 2 diabetes were pre-conditioned with 30µM of RFYVVMWK (or truncated peptide RFYVVM. CD34(+) cell adhesion was assessed on a vitronectin-collagen matrix and on a TNFα or IL-1β- stimulated HUVEC monolayers. Adhesion receptors, platelet/CD34(+) cell conjugates, and cell viability were analyzed by flow cytometry and confocal microscopy.Results: RFYVVMWK increased by 8 folds the adhesion of T2D CD34(+) cells to the vitronectin-collagen matrix (p Conclusions: Priming CD34(+) cells with RFYVVMWK may enhance their vascular engraftment during autologous pro-angiogenic cell therapy..

Published
2016
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4. Baseline sensitivity of T cells to alpha-IFN correlates with sustained virological response to IFN-based triple therapy in HCV infection

Author

Christophe Hézode, Cécile Alanio, G. Uze, Armanda Casrouge, Vincent Mallet, I. Rosa-Hézode, P. Pellet, Estelle Mottez, Matthew L. Albert, Philippe Renard, Stanislas Pol, Philippe Sultanik, Laurence Bousquet, Institut Cochin (IC UM3 (UMR 8104 / U1016)), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Immunobiologie des Cellules Dendritiques, Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre d'Immunologie Humaine (CIH), Service d'hépato-gastro-entérologie [APHP Henri Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Centre Hospitalier Victor Dupouy, CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Dynamique des interactions membranaires normales et pathologiques (DIMNP), Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université Montpellier 1 (UM1), Service d'hépatologie médicale [CHU Cochin], Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), This work was supported by grants from the Agence Nationale de Recherche sur le SIDA et les Hépatites Virales (ANRS 11416) and ERC Starting award (M.A.). We thank the Fondation pour la Recherche Médicale for master and PhD student bursaries, We thank the Fondation pour la Recherche Médicale for master and PhD student bursaries, the Etablissement Français du Sang (EFS) for healthy donors samples, S. Pellegrini for critical review, S. Feton and K. Sperber for coordination of the clinical protocol, J. Gaston, S. Lagaye and M. Andrieu for technical assistance. We would also like to acknowledge the Department of Development, Reproduction and Cancer, Institut Cochin, Paris, the Department of Immunology, Institut Cochin, Paris, and the Centre d'Immunologie Humaine (CIH), Institut Pasteur, Paris, for support and technical expertise, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), CHU Pitié-Salpêtrière [APHP], CHU Cochin [AP-HP]-Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Institut Cochin (UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Centre National de la Recherche Scientifique (CNRS), Institut Pasteur [Paris] - Institut National de la Santé et de la Recherche Médicale (INSERM), Assistance publique - Hôpitaux de Paris (AP-HP) - Hôpital Henri Mondor - Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Université Montpellier 1 (UM1) - Université Montpellier 2 - Sciences et Techniques (UM2) - Université de Montpellier (UM) - Centre National de la Recherche Scientifique (CNRS), and Assistance publique - Hôpitaux de Paris (AP-HP) - CHU Cochin [AP-HP]

Subjects
Male, MESH: T-Lymphocytes/metabolism, T-Lymphocytes, Drug Resistance, MESH: Hepatitis C, Chronic/virology, MESH: Leukocytes, Mononuclear/drug effects, Telaprevir, chemistry.chemical_compound, Pegylated interferon, Phosphorylation, MESH: Treatment Outcome, MESH: Aged, MESH: STAT1 Transcription Factor/metabolism, MESH: Middle Aged, biology, MESH: Polymorphism, Single Nucleotide, IFNα desensitization, IFN-based triple therapy, MESH: T-Lymphocytes/immunology, Middle Aged, Viral Load, MESH: Antiviral Agents/pharmacology, MESH: Interleukins/genetics, MESH: Case-Control Studies, 3. Good health, STAT1 Transcription Factor, Treatment Outcome, Infectious Diseases, MESH: Interferon-alpha/therapeutic use, [SDV.IMM]Life Sciences [q-bio]/Immunology, Drug Therapy, Combination, Female, MESH: Viral Load, medicine.drug, MESH: Leukocytes, Mononuclear/metabolism, MESH: Hepatitis C, Chronic/drug therapy, [SDV.IMM] Life Sciences [q-bio]/Immunology, CD3, MESH: T-Lymphocytes/drug effects, T cells, Alpha interferon, Antiviral Agents, Polymorphism, Single Nucleotide, Peripheral blood mononuclear cell, Virology, Boceprevir, medicine, Humans, Aged, MESH: Hepatitis C, Chronic/immunology, MESH: Humans, Hepatology, MESH: Phosphorylation, business.industry, Interleukins, Ribavirin, MESH: Drug Resistance/genetics, Interferon-alpha, Hepatitis C, Chronic, MESH: Male, MESH: Drug Therapy, Combination, MESH: Interferon-alpha/pharmacology, chemistry, MESH: Leukocytes, Mononuclear/immunology, Case-Control Studies, Immunology, MESH: Antiviral Agents/therapeutic use, Leukocytes, Mononuclear, biology.protein, chronic HCV infection, Interferons, business, MESH: Female, Ex vivo, MESH: Hepatitis C, Chronic/genetics
Abstract

International audience; Chronic infection with HCV is a public health problem with approximately 170 million people infected worldwide. Interferon alpha (IFNα) sensitivity in liver and IL28B genotype has been identified as important determinants of HCV clearance in the setting of pegylated interferon/ribavirin treatment. Herein, we explored IFNα sensitivity in PBMC from 21 healthy donors and 21 HCV-infected patients treated with pegylated interferon/ribavirin and HCV nonstructural protein-3 inhibitors (i.e. telaprevir/boceprevir). We explored phospho-STAT1 level as read-out for IFN signalling pathway activation in PBMC, T cells and monocytes and correlated results with virological response. We found that PBMC from healthy donors are desensitized to IFNα after priming and challenged with IFNα, with a subsequent decrease of phospho-STAT1 and interferon-stimulated genes. Furthermore, we show that CD3+ T cells, but not monocytes, become desensitized after 4 weeks of treatment, with a significant decrease of phospho-STAT1 after ex vivo IFNα stimulation. Finally, we identified baseline phospho-STAT1 level in CD3+ T cells as a potential biomarker of sustained virological response, regardless of the IL28B genotype. In the upcoming costly era of IFN-sparing regimen, baseline IFNα sensitivity could act as biomarker to define cost-effectiveness strategies of treatment by identifying patients who will or will not respond to IFN-based treatments.

Published
2015
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5. Low DPP4 expression and activity in multiple sclerosis

Author

Rocío Ramos-Medina, Bárbara Alonso, Armanda Casrouge, Janet Vega, Matthew L. Albert, Marta Tejera-Alhambra, Silvia Sánchez-Ramón, Clara de Andrés, Department of Immunology, Hospital General Universitario Gregorio Marañón, Centre d'Immunologie Humaine (CIH), Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of neurology, Center Alicia Koplowitz for Multiple Sclerosis of the Community of Madrid, Immunobiologie des Cellules Dendritiques, This work was supported by grants from the Fundación Mapfre, the Fundación Salud 2000 prize for MS research (SSR) and the European Research Council Starting Award (MLA). Marta Tejera-Alhambra received an EFIS grant in 2011 for her stay at Institut Pasteur in Paris., and Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Male, Lymphocyte Activation, 0302 clinical medicine, T-Lymphocyte Subsets, MESH: Receptors, Antigen, T-Cell/metabolism, Immunology and Allergy, Vitamin D, 0303 health sciences, MESH: Middle Aged, Middle Aged, Pathophysiology, MESH: Reproducibility of Results, Phenotype, medicine.anatomical_structure, Biomarker (medicine), MESH: Multiple Sclerosis/genetics, [SDV.IMM]Life Sciences [q-bio]/Immunology, Female, Adult, MESH: Leukocytes, Mononuclear/metabolism, Immunology, Central nervous system, Receptors, Antigen, T-Cell, Biology, Dipeptidyl peptidase 4, MESH: Phenotype, Multiple sclerosis, 03 medical and health sciences, Sex Factors, MESH: Sex Factors, Clinical activity, MESH: T-Lymphocyte Subsets/immunology, medicine, Humans, MESH: Multiple Sclerosis/metabolism, MESH: Vitamin D/blood, MESH: Dipeptidyl Peptidase 4/genetics, Dipeptidyl peptidase-4, 030304 developmental biology, CD26, MESH: Multiple Sclerosis/diagnosis, Autoimmune disease, MESH: Humans, MESH: Biomarkers/metabolism, Reproducibility of Results, MESH: Adult, Plasma levels, Biomarker, MESH: ROC Curve, medicine.disease, MESH: Male, MESH: Lymphocyte Activation/immunology, MESH: Dipeptidyl Peptidase 4/metabolism, ROC Curve, Leukocytes, Mononuclear, MESH: T-Lymphocyte Subsets/metabolism, MESH: Female, Biomarkers, 030217 neurology & neurosurgery, CD8
Abstract

International audience; Multiple sclerosis (MS) is a prototypic Th1/Th17 chronic autoimmune disease of the central nervous system. Dipeptidyl peptidase 4 (DPP4 or CD26) is a multifunctional molecule involved in autoimmune diseases' pathophysiology. We sought to integrate disparate pieces of data and analyze the plasma levels of sDPP4, DPP activity and DPP4 surface expression on T-cells in 129 MS patients with different clinical forms and 53 healthy controls, across two independent cohorts. Herein, we provide new evidence that sDPP4 concentration and DPP activity are significantly lower in MS patients than controls (p < 0.0001 and p < 0.01, respectively). In contrast, the frequency of circulating CD8(+)DPP4(hi) T-cells (p = 0.02) was increased in MS patients. This is the first study that simultaneously analyzes DPP4 expression and function in a large cohort of MS patients. Our data indicate a putative role for DPP4 in MS pathophysiology and suggest that a deeper understanding of surface versus shed DPP4 biology is warranted.

Published
2013
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6. Simultaneous assessment of autophagy and apoptosis using multispectral imaging cytometry

Author

Matthew L. Albert, Claire De La Calle, Milena Hasan, Pierre-Emmanuel Joubert, Helen K. W. Law, Centre d'Immunologie Humaine (CIH), Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Supported by grants from ARC (equipment grant to the Centre d’Immunologie Humaine), the Canceropole, Région Ile de France (C.C.), the EURYI Award from the European Science Foundation and the Young Investigator Award from the European Research Council (M.L.A.)., and Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Time Factors, MESH: Fibroblasts/cytology, new methodology, MESH: Fibroblasts/metabolism, Apoptosis, multispectral imaging cytometry, Mutually exclusive events, MESH: Leukocytes, Mononuclear/drug effects, MESH: Apoptosis/radiation effects, Mice, MESH: Image Cytometry/methods, MESH: Animals, Image Cytometry, 0303 health sciences, MESH: Lysosomes/radiation effects, 030302 biochemistry & molecular biology, Chloroquine, Cell biology, Blot, MESH: Autophagy/radiation effects, [SDV.IMM]Life Sciences [q-bio]/Immunology, influenza, MESH: Lysosomes/drug effects, Microtubule-Associated Proteins, Signal Transduction, MESH: Leukocytes, Mononuclear/metabolism, Programmed cell death, MESH: Apoptosis/drug effects, Ultraviolet Rays, MESH: Leukocytes, Mononuclear/cytology, Multiple stress, Biology, Cellular level, 03 medical and health sciences, MESH: Signal Transduction/drug effects, Autophagy, Animals, Humans, MESH: Fibroblasts/radiation effects, MESH: Mice, Molecular Biology, MESH: Chloroquine/pharmacology, 030304 developmental biology, MESH: Humans, MESH: Signal Transduction/radiation effects, MESH: Autophagy/drug effects, MESH: Leukocytes, Mononuclear/radiation effects, MESH: Time Factors, Cell Biology, Fibroblasts, Embryo, Mammalian, MESH: Lysosomes/metabolism, MESH: Fibroblasts/drug effects, MESH: Microtubule-Associated Proteins/metabolism, Leukocytes, Mononuclear, MESH: Ultraviolet Rays, MESH: Embryo, Mammalian/cytology, Lysosomes, Cytometry
Abstract

International audience; Multiple stress pathways result in the induction of autophagy and apoptosis. Current methods (e.g., protein gel blot, microscopy) do not offer quantitative single-cell resolution, thus making it difficult to discern if these pathways are mutually exclusive or, in some situations, cooperative in executing cell death. We report a novel method that enables high-throughput, high-content assessment of LC3 puncta and caspase-3 cleavage at the single cell level.

Published
2011
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