Article abstract
Nature Immunology 8, 825 - 834 (2007)
Published online: 24 June 2007 | doi:10.1038/ni1482
Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death
Marta A Toscano1,6, Germán A Bianco1,6,7, Juan M Ilarregui1,6,7, Diego O Croci1,6, Jorge Correale2, Joseph D Hernandez3, Norberto W Zwirner1,6, Francoise Poirier4, Eleanor M Riley5, Linda G Baum3 & Gabriel A Rabinovich1,6
Abstract
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.
- División de Immunogenética. Hospital de Clínicas 'José de San Martín', Facultad de Medicina, Universidad de Buenos Aires, C1120AAF Buenos Aires, Argentina.
- Departamento de Neurología, Instituto de Investigaciones Neurológicas 'Dr. Raul Carrea', C1428 Buenos Aires, Argentina.
- Department of Pathology and Laboratory Medicine, University of California at Los Angeles School of Medicine, Los Angeles, California 90095, USA.
- Institut Jacques Monod, Unités Mixtes de Recherche-Centre National de la Recherche Scientifique 7592, Paris 6 and Paris 7 Universities, 75251 Paris, France.
- Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London WC1 E7HT, UK.
- Present address: Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas and Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, C1428ADN Buenos Aires, Argentina.
- These authors equally contributed to this work.
Correspondence to: Gabriel A Rabinovich1,6 e-mail: gabyrabi@ciudad.com.ar
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