Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death
| Autor: | Marta A. Toscano, Diego O. Croci, Germán A Bianco, Juan M. Ilarregui, Linda G. Baum, Eleanor M. Riley, Jorge Correale, Joseph D. Hernandez, Gabriel A. Rabinovich, Norberto Walter Zwirner, Françoise Poirier |
|---|---|
| Přispěvatelé: | División Inmunogenética [Buenos Aires], Departamento de Microbiología [Buenos Aires], Facultad de Medicina [Buenos Aires], Universidad de Buenos Aires [Buenos Aires] (UBA)-Universidad de Buenos Aires [Buenos Aires] (UBA)-Facultad de Medicina [Buenos Aires], Universidad de Buenos Aires [Buenos Aires] (UBA)-Universidad de Buenos Aires [Buenos Aires] (UBA)-Hospital de Clínicas 'José de San Martín' [Buenos Aires], Departamento de Neurologia, Instituto de Investigaciones Neurológicas 'Dr. Raul Carrea', Instituto de Investigaciones Neurológicas 'Dr. Raul Carrea', Department of Pathology and Laboratory Medicine [UCLA], University of California [Los Angeles] (UCLA), University of California-University of California-School of Medicine, Institut Jacques Monod (IJM (UMR_7592)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Department of Infectious and Tropical Diseases (LSHTM), London School of Hygiene and Tropical Medicine (LSHTM) |
| Rok vydání: | 2007 |
| Předmět: |
MESH: Inflammation
Glycosylation Galectin 1 MESH: Interleukin-17 MESH: Membrane Glycoproteins MESH: Flow Cytometry Apoptosis MESH: T-Lymphocyte Subsets Mice Interleukin 21 chemistry.chemical_compound 0302 clinical medicine T-Lymphocyte Subsets Immunology and Allergy Cytotoxic T cell MESH: Animals MESH: In Situ Nick-End Labeling [SDV.BDD]Life Sciences [q-bio]/Development Biology 0303 health sciences Membrane Glycoproteins MESH: Immunoblotting Effector Interleukin-17 Cell Differentiation T-Lymphocytes Helper-Inducer MESH: Glycosylation Flow Cytometry Adoptive Transfer Cell biology medicine.anatomical_structure Interleukin 13 Galectin-1 [SDV.IMM]Life Sciences [q-bio]/Immunology MESH: Cell Differentiation Encephalomyelitis Autoimmune Experimental T cell Immunoblotting Immunology Biology 03 medical and health sciences Th2 Cells MESH: Th2 Cells Polysaccharides In Situ Nick-End Labeling medicine Animals Humans MESH: T-Lymphocytes Helper-Inducer MESH: Encephalomyelitis Autoimmune Experimental Antigen-presenting cell MESH: Mice 030304 developmental biology MESH: Galectin 1 Inflammation MESH: Humans MESH: Apoptosis Th1 Cells Molecular biology carbohydrates (lipids) MESH: Adoptive Transfer MESH: Polysaccharides MESH: Th1 Cells chemistry 030215 immunology |
| Zdroj: | Nature Immunology Nature Immunology, Nature Publishing Group, 2007, 8 (8), pp.825-34. ⟨10.1038/ni1482⟩ |
| ISSN: | 1529-2916 1529-2908 |
| DOI: | 10.1038/ni1482 |
| Popis: | International audience; Regulated glycosylation controls T cell processes, including activation, differentiation and homing by creating or masking ligands for endogenous lectins. Here we show that stimuli promoting T helper type 1 (TH1), TH2 or interleukin 17-producing T helper (TH-17) differentiation can differentially regulate the glycosylation pattern of T helper cells and modulate their susceptibility to galectin-1, a glycan-binding protein with anti-inflammatory activity. Although TH1- and TH-17-differentiated cells expressed the repertoire of cell surface glycans critical for galectin-1-induced cell death, TH2 cells were protected from galectin-1 through differential sialylation of cell surface glycoproteins. Consistent with those findings, galectin-1-deficient mice developed greater TH1 and TH-17 responses and enhanced susceptibility to autoimmune neuroinflammation. Our findings identify a molecular link among differential glycosylation of T helper cells, susceptibility to cell death and termination of the inflammatory response. |
| Databáze: | OpenAIRE |
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