Evidence map›Paper›PMID 42593965›Full record

ArticleCell reports2026

Dietary vitamin A restricts intestinal tuft cell differentiation.

Bailey J Didriksen, Emily M Eshleman, Taylor Rice, Amanda Waddell, Shikha Negi, Laura Engleman, Seika Hashimoto-Hill, Rebekah Karns, Mark R Frey, Theresa Alenghat

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Bailey J DidriksenDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Immunology Graduate Program, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Emily M EshlemanDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. Electronic address: emily.eshleman@cchmc.org.
Taylor RiceDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Amanda WaddellDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Shikha NegiDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Laura EnglemanDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Seika Hashimoto-HillDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Rebekah KarnsDivision of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Mark R FreyThe Saban Research Institute, Children's Hospital Los Angeles, Los Angeles, CA, USA; Department of Pediatrics and Department of Biochemistry and Molecular Biology, University of Southern California Keck School of Medicine, Los Angeles, CA, USA.
Theresa AlenghatDivision of Immunobiology, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Center for Inflammation and Tolerance, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. Electronic address: theresa.alenghat@cchmc.org.

Funding

Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Kathryn Ann Wikenheiser-Brokamp · 2007 to 2026
$24.4M
Xenotransplant and Genome Editing CoreU54DK126108 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Daniel Starczynowski, YI ZHENG · 2021 to 2026
$5.0M
Host integration of commensal and pathogenic bacterial-derived signalsR01DK116868 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Theresa Alenghat · 2018 to 2026
$4.1M
Epigenetic regulation of intestinal tuft cellsR01DK137771 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Theresa Alenghat · 2024 to 2026
$2.5M
The role of SPRY2 in the colonic epithelial response to inflammationR01DK119694 · NIDDK · CHILDREN'S HOSPITAL OF LOS ANGELES · PI FREY, MARK R · 2019 to 2022
$1.5M
Commensal bacterial metabolism of dietary phytate in host defenseK08DK134884 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Seika Hashimoto-Hill · 2023 to 2026
$622k
Microbial regulation of intestinal tuft cell homeostasisK01DK135647 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Emily M. Eshleman · 2023 to 2026
$563k
NIDDK NIH HHS K01 DK135647NIDDK NIH HHS K08 DK134884NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK116868NIDDK NIH HHS R01 DK119694NIDDK NIH HHS R01 DK137771NIDDK NIH HHS U54 DK126108
6 · The paper itself

Abstract

Despite evidence highlighting immunoregulatory roles of tuft cells, it is not known whether vitamin A or retinoic acid affects tuft cell homeostasis. Here, we find that epithelial-intrinsic retinoic acid receptor regulates tuft cell numbers in mice. However, loss of retinoic acid signaling in tuft cells does not replicate this effect, suggesting altered differentiation. Consistent with this, retinoic acid administration to stem cell-derived organoids reduces tuft cell numbers, and epithelial-intrinsic retinoic acid is sufficient to alter tuft cell responses. In addition, dietary vitamin A dynamically alters tuft cells in vivo and regulates anti-helminth immunity in a tuft cell-dependent manner. Mechanistically, epithelial retinoic acid signaling promotes expression of Sprouty2, a negative regulator of tuft cell differentiation. Furthermore, stem cell-specific Sprouty2 disruption abrogates vitamin A regulation of tuft cells. Collectively, these data indicate that retinoic acid restricts tuft cell differentiation and carries important implications for how vitamin A affects intestinal health and immunity.

Indexed as

CP: metabolismCP: stem cell researchDietDifferentiationEpithelialILCIntestineRetinoic acidStem cellTuft cellVitamin A

Identifiers

PMID42593965
PMCPMC13589826

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.