Differential glycosylation of T(H)1, T(H)2 and T(H)-17 effector cells selectively regulates susceptibility to cell death.


Toscano, MA; Bianco, GA; Ilarregui, JM; Croci, DO; Correale, J; Hernandez, JD; Zwirner, NW; Poirier, F; Riley, EM; Baum, LG; Rabinovich, GA; (2007) Differential glycosylation of T(H)1, T(H)2 and T(H)-17 effector cells selectively regulates susceptibility to cell death. Nature immunology, 8 (8). pp. 825-834. ISSN 1529-2908 DOI: https://doi.org/10.1038/ni1482

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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 (T(H)1), T(H)2 or interleukin 17-producing T helper (T(H)-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 T(H)1- and T(H)-17-differentiated cells expressed the repertoire of cell surface glycans critical for galectin-1-induced cell death, T(H)2 cells were protected from galectin-1 through differential sialylation of cell surface glycoproteins. Consistent with those findings, galectin-1-deficient mice developed greater T(H)1 and T(H)-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.

Item Type: Article
Faculty and Department: Faculty of Infectious and Tropical Diseases > Dept of Immunology and Infection
Research Centre: Malaria Centre
PubMed ID: 17589510
Web of Science ID: 248169400010
URI: http://researchonline.lshtm.ac.uk/id/eprint/9347

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