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Publication : Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death.

First Author  Toscano MA Year  2007
Journal  Nat Immunol Volume  8
Issue  8 Pages  825-34
PubMed ID  17589510 Mgi Jnum  J:123416
Mgi Id  MGI:3718280 Doi  10.1038/ni1482
Citation  Toscano MA, et al. (2007) Differential glycosylation of T(H)1, T(H)2 and T(H)-17 effector cells selectively regulates susceptibility to cell death. Nat Immunol 8(8):825-834
abstractText  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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