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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| Auteurs principaux: | , , , , , , |
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| Format: | article |
| Langue: | EN |
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Public Library of Science (PLoS)
2019
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| Accès en ligne: | https://doaj.org/article/60517fbf723743b2b183094b3a13e13c |
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