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

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 (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.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Toscano MA,Bianco GA,Ilarregui JM,Croci DO,Correale J,Hernandez JD,Zwirner NW,Poirier F,Riley EM,Baum LG,Rabinovich GA

doi

10.1038/ni1482

subject

Has Abstract

pub_date

2007-08-01 00:00:00

pages

825-34

issue

8

eissn

1529-2908

issn

1529-2916

pii

ni1482

journal_volume

8

pub_type

杂志文章

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