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. |