Fucose-specific DC-SIGN signalling directs T helper cell type-2 responses via IKKε- and CYLD-dependent Bcl3 activation
作者： Sonja I. Gringhuis , Tanja M. Kaptein , Brigitte A. Wevers , Annelies W. Mesman , Teunis B. H. Geijtenbeek
DOI: 10.1038/NCOMMS4898
关键词:
摘要: Carbohydrate-specific signalling through DC-SIGN provides dendritic cells with plasticity to tailor immunity the nature of invading microbes. Here we demonstrate that recognition fucose-expressing extracellular pathogens like Schistosoma mansoni and Helicobacter pylori by favors T helper cell type-2 (TH2) responses via activation atypical NF-κB family member Bcl3. Crosstalk between TLR results in TLR-induced MK2-mediated phosphorylation LSP1, associated DC-SIGN, upon fucose binding. Subsequently, IKKe CYLD are recruited phosphorylated LSP1. is pivotal for suppression deubiquitinase activity subsequent nuclear translocation ubiquitinated Bcl3 represses proinflammatory cytokine expression, while enhancing interleukin-10 (IL-10) TH2-attracting chemokine shifting TH differentiation from TH1 TH2 polarization. Thus, directs adaptive an IKKe-CYLD-dependent pathway leading activation, which might be targeted vaccination strategies or prevent aberrant inflammation allergy.
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