Evidence map›Paper›PMID 40995824›Full record

ArticleGut microbes2025

Tryptophan catabolites from microbiota ameliorate immune-mediated hepatitis through activating aryl hydrocarbon receptor of T cells.

Bo Li, Xueying Liang, Yikang Li, Rui Wang, Yiran Wei, Qiaoyan Liu, Jun Zhang, Qixia Wang, Qi Miao, Xiao Xiao and 7 more

Abstract read
In one paragraph

Article in Gut microbes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
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  3. Experimental Models of Autoimmune Hepatitis: Disease Fidelity and Translational Relevance.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
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  5. Article
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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

17 authors.

Bo LiNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Xueying LiangNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Yikang LiNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Rui WangNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Yiran WeiNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Qiaoyan LiuNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Jun ZhangNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Qixia WangNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Qi MiaoNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Xiao XiaoNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Min LianNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Zhi WangGuanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Stomatological Hospital, Sun Yat-Sen University, Guangzhou, China.
Yufeng ZhouInstitute of Pediatrics, Children's Hospital of Fudan University, Shanghai, China.
M Eric GershwinDivision of Rheumatology, Department of Medicine, Allergy and Clinical Immunology, University of California at Davis, Davis, CA, USA.
Zhengrui YouNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Ruqi TangNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.
Xiong MaNHC Key Laboratory of Digestive Diseases (Renji Hospital, Shanghai Jiaotong University School of Medicine), Division of Gastroenterology and Hepatology, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai JiaoTong University; Shanghai Institute of Digestive Disease;145 Middle Shandong Road, Shanghai 200001, China.ORCID 0000-0001-9616-4672

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal dysbiosis and T cell-mediated immune attack are implicated in the pathogenesis of autoimmune hepatitis (AIH). However, the mechanisms by which microbiota-derived metabolites modulate immune homeostasis in AIH remain elusive. Here, we demonstrated that microbiota-derived indole-3-carboxaldehyde (ICA) was significantly reduced in patients with AIH. Treatment with ICA restricted the activation of effector T cells by activating AhR in T lymphocytes. Nuclear translocation of AhR induced the transcription of PI3K interacting protein 1 (Pik3ip1), which inhibited the PI3K/Akt/mTOR signaling pathway. In vivo supplementation of ICA suppressed effector T cells and mitigated the tissue damage and hepatic inflammation in two mouse models of T cell-mediated hepatitis. Importantly, T cell-specific deletion of AhR abrogated the protective effects of ICA in AIH-like mouse model. Finally, administration of Lactobacillus reuteri resulted in elevated level of ICA and protected mice from liver damage. Our data suggest that ICA supplementation ameliorates immune-mediated hepatitis through agonizing AhR in T cells, presenting a promising therapeutic strategy for AIH.

Indexed as

Gastrointestinal MicrobiomeHepatitis, AutoimmuneIndolesReceptors, Aryl HydrocarbonT-LymphocytesTryptophanAnimalsDisease Models, AnimalFemaleHumansLimosilactobacillus reuteriMaleMiceMice, Inbred C57BLSignal Transductionindole-3-carbaldehydeIndolesReceptors, Aryl HydrocarbonTryptophanaryl hydrocarbon receptorimmune-mediated hepatitisIndole-3-carboxaldehydelactobacillus reuteriPI3K interacting protein 1

Identifiers

PMID40995824
PMCPMC12477874

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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.