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- W2912233211 abstract "Microfold cells (M-cells) are specialized cells of the intestine that sample luminal microbiota and dietary antigens to educate the immune cells of the intestinal lymphoid follicles. The function of M-cells in systemic inflammatory responses are still unclear. Here we show that epithelial non-canonical NFkB signaling mediated by NFkB-inducing kinase (NIK) is highly active in intestinal lymphoid follicles, and is required for M-cell maintenance. Intestinal NIK signaling modulates M-cell differentiation and elicits both local and systemic IL-17A and IgA production. Importantly, intestinal NIK signaling is active in mouse models of colitis and patients with inflammatory bowel diseases; meanwhile, constitutive NIK signaling increases the susceptibility to inflammatory injury by inducing ectopic M-cell differentiation and a chronic increase of IL-17A. Our work thus defines an important function of non-canonical NFkB and M-cells in immune homeostasis, inflammation and polymicrobial sepsis." @default.
- W2912233211 created "2019-02-21" @default.
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- W2912233211 date "2019-02-08" @default.
- W2912233211 modified "2023-10-18" @default.
- W2912233211 title "Intestinal non-canonical NFκB signaling shapes the local and systemic immune response" @default.
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- W2912233211 doi "https://doi.org/10.1038/s41467-019-08581-8" @default.
- W2912233211 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6368617" @default.
- W2912233211 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30737385" @default.
- W2912233211 hasPublicationYear "2019" @default.
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