ArticleCell host & microbe2026
The gut microbiota directs vitamin A flux to regulate intestinal T cell development.
Article in Cell host & microbe, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- ADH1C Down-Regulation Is a Key Hypoxia Response in Colon Epithelium.The American journal of pathology · 2026Article
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17 authors.
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Abstract
The intestinal microbiota shapes adaptive immunity, but the mechanisms remain incompletely defined. Here, we show that the microbiota initiates movement of retinoids-dietary vitamin A derivatives including retinol and retinoic acid-through a sequential pathway from epithelial cells to myeloid cells and ultimately to T cells in the mesenteric lymph nodes (mLNs). This cellular axis is traversed over three days. Microbe-associated molecular patterns initiate retinoid flux by inducing expression of serum amyloid A proteins. These epithelial retinol-binding proteins are necessary and sufficient for epithelial-to-myeloid retinoid transfer and myeloid cell migration to the mLNs. In the mLNs, microbial antigen drives retinoid transfer from myeloid cells to developing T cells, culminating in T cell retinoid uptake and transcriptional programming. This pathway is activated during postnatal development, when gut adaptive immunity is established. These findings reveal that the microbiota programs intestinal adaptive immunity by regulating immune cell access to a nutrient-derived developmental signal.
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