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- W3043422039 abstract "B cell depletion potently reduces episodes of inflammatory demyelination in multiple sclerosis (MS), predominantly through loss of innate rather than adaptive immunity. However, molecular mechanisms controlling innate versus adaptive B cell function are poorly understood. N-glycan branching, via interactions with galectins, controls endocytosis and signaling of cell surface receptors to control cell function. Here we report that N-glycan branching in B cells dose dependently reduces pro-inflammatory innate responses by titrating decreases in Toll-like receptor-4 (TLR4) and TLR2 surface expression via endocytosis. In contrast, a minimal level of N-glycan branching maximizes surface retention of the B cell receptor (BCR) and the CD19 co-receptor to promote adaptive immunity. Branched N-glycans inhibit antigen presentation by B cells to reduce T helper cell-17 (TH17)/TH1 differentiation and inflammatory demyelination in mice. Thus, N-glycan branching negatively regulates B cell innate function while promoting/maintaining adaptive immunity via BCR, providing an attractive therapeutic target for MS." @default.
- W3043422039 created "2020-07-23" @default.
- W3043422039 creator A5016878204 @default.
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- W3043422039 creator A5033797204 @default.
- W3043422039 creator A5072430706 @default.
- W3043422039 creator A5084224456 @default.
- W3043422039 date "2020-08-01" @default.
- W3043422039 modified "2023-09-30" @default.
- W3043422039 title "N-Glycan Branching Decouples B Cell Innate and Adaptive Immunity to Control Inflammatory Demyelination" @default.
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- W3043422039 doi "https://doi.org/10.1016/j.isci.2020.101380" @default.
- W3043422039 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7398982" @default.
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- W3043422039 hasPublicationYear "2020" @default.
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