References
Query Results -- Details
MGI Accession ID: MGI:3718280
J Number: J:123416
Other Accession IDs:
Title: Differential glycosylation of T(H)1, T(H)2 and T(H)-17 effector cells selectively regulates susceptibility to cell death.
Authors: Toscano MA; Bianco GA; Ilarregui JM; Croci DO; Correale J; Hernandez JD; Zwirner NW; Poirier F; Riley EM; Baum LG; Rabinovich GA
Journal: Nat Immunol
Volume: 8
Issue: 8
Date: 2007 Aug
Year: 2007
Pages: 825-834
Review Status: Peer Reviewed
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.
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