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

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Toscano, Marta A | Bianco, Germán A | Ilarregui, Juan M | Croci, Diego O | Correale, Jorge | Hernandez, Joseph D | Zwirner, Norberto W | Poirier, Francoise | Riley, Eleanor M | Baum, Linda G | Rabinovich, Gabriel A

Edité par CCSD ; Nature Publishing Group -

International audience. 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.

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