Evidence map›Paper›PMID 39432783›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2024

The pyruvate-GPR31 axis promotes transepithelial dendrite formation in human intestinal dendritic cells.

Eri Oguro-Igashira, Mari Murakami, Ryota Mori, Ryuichi Kuwahara, Takako Kihara, Masaharu Kohara, Makoto Fujiwara, Daisuke Motooka, Daisuke Okuzaki, Mitsuru Arase and 10 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Dietary Antigen Interaction with Intestinal Epithelial Cells.Current allergy and asthma reports · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. The pyruvate-GPR31 axis promotes transepithelial dendrite formation in human intestinal dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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

20 authors.

Eri Oguro-IgashiraDepartment of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.
Mari MurakamiDepartment of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0001-6458-8235
Ryota MoriDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.
Ryuichi KuwaharaDepartment of Gastroenterological Surgery, Division of Inflammatory Bowel Disease Surgery, Hyogo Medical University, Hyogo 663-8501, Japan.ORCID 0000-0001-7599-6330
Takako KiharaDepartment of Surgical Pathology, Hyogo Medical University, Hyogo 663-8501, Japan.ORCID 0000-0002-0954-2733
Masaharu KoharaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0009-0006-7636-5833
Makoto FujiwaraDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0002-6799-9774
Daisuke MotookaWorld Premier International Research Center Initiative (WPI) Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.
Daisuke OkuzakiWorld Premier International Research Center Initiative (WPI) Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0002-4552-783X
Mitsuru AraseDepartment of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0003-3944-0698
Hironobu ToyotaDepartment of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0009-0005-5351-9433
Siyun PengDepartment of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0009-0004-2422-3855
Takayuki OginoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0001-5435-4144
Yasuji KitabatakeDepartment of Pediatrics, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0002-2907-9512
Eiichi MoriiDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0001-8490-3650
Seiichi HirotaDepartment of Surgical Pathology, Hyogo Medical University, Hyogo 663-8501, Japan.
Hiroki IkeuchiDepartment of Gastroenterological Surgery, Division of Inflammatory Bowel Disease Surgery, Hyogo Medical University, Hyogo 663-8501, Japan.ORCID 0000-0001-9144-5782
Eiji UmemotoLaboratory of Microbiology and Immunology, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka 422-8526, Japan.
Atsushi KumanogohDepartment of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.ORCID 0000-0003-4749-7117
Kiyoshi TakedaDepartment of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan.

Funding

BD Biosciences (Becton Dickenson Biosciences) J178501002Japan Agency for Medical Research and Development (AMED) JP21gm1010004MEXT | Japan Society for the Promotion of Science (JSPS) JP21H050430MEXT | Japan Society for the Promotion of Science (JSPS) JP21K07895MEXT | Japan Society for the Promotion of Science (JSPS) JPMJSP213
6 · The paper itself

Abstract

The intestinal lumen is rich in gut microbial metabolites that serve as signaling molecules for gut immune cells. G-protein-coupled receptors (GPCRs) sense metabolites and can act as key mediators that translate gut luminal signals into host immune responses. However, the impacts of gut microbe-GPCR interactions on human physiology have not been fully elucidated. Here, we show that GPR31, which is activated by the gut bacterial metabolite pyruvate, is specifically expressed on type 1 conventional dendritic cells (cDC1s) in the lamina propria of the human intestine. Using human induced pluripotent stem cell-derived cDC1s and a monolayer human gut organoid coculture system, we show that cDC1s extend their dendrites toward pyruvate on the luminal side, forming transepithelial dendrites (TED). Accordingly, GPR31 activation via pyruvate enhances the fundamental function of cDC1 by allowing efficient uptake of gut luminal antigens, such as dietary compounds and bacterial particles through TED formation. Our results highlight the role of GPCRs in tuning the human gut immune system according to local metabolic cues.

Indexed as

Dendritic CellsPyruvic AcidReceptors, G-Protein-CoupledDendritesGastrointestinal MicrobiomeHumansInduced Pluripotent Stem CellsIntestinal MucosaIntestinesOrganoidsSignal TransductionPyruvic AcidReceptors, G-Protein-Coupledantigen recognitiondendritic cellGPR31G protein-coupled receptorstransepithelial dendrite formation

Identifiers

PMID39432783
PMCPMC11536072

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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.