Increasing cell permeability of N-acetylglucosamine via 6-acetylation enhances capacity to suppress T-helper 1 (TH1)/TH17 responses and autoimmunity.

N-acetylglucosamine (GlcNAc) branching of Asn (N)-linked glycans inhibits pro-inflammatory T cell responses and models of autoimmune diseases such as Multiple Sclerosis (MS). Metabolism controls N-glycan branching in T cells by regulating de novo hexosamine pathway biosynthesis of UDP-GlcNAc, the do...

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Main Authors: Sung-Uk Lee, Carey F Li, Christie-Lynn Mortales, Judy Pawling, James W Dennis, Ani Grigorian, Michael Demetriou
Format: article
Language:EN
Published: Public Library of Science (PLoS) 2019
Subjects:
R
Q
Online Access:https://doaj.org/article/60517fbf723743b2b183094b3a13e13c
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