DIFFERENTIAL GLYCOSYLATION OF TH1, TH2 AND TH-17 EFFECTOR CELLS SELECTIVELY REGULATES SUSCEPTIBILITY TO CELL DEATH

MARTA A. TOSCANO,; GERMAN A. BIANCO; JUAN M. ILARREGUI; DIEGO CROCI,; JORGE CORREALE,; JOSEPH HERNANDEZ,; NORBERTO W. ZWIRNER,; FRANCOISE POIRIER,; ELEANOR RILEY,; LINDA G. BAUM,; GABRIEL A. RABINOVICH

NATURE IMMUNOLOGY

Nature America Inc.

Año: 2007 vol. 8 p. 825 - 834

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.8(8):825-34