Evidence map›Paper›PMID 41780884›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

Ubiquitin-Conjugating Enzyme E2O Primes Hepatocytes to Restore Immune Tolerance in Autoimmune Hepatitis via Inhibiting Y-Box Binding Protein 1/Interleukin-6 Axis.

Yu Lei, Han Wang, Yu Chen, Shuhui Wang, Zhipeng Du, Zheng Huang, Muru Wang, Shangshu Nie, Ping Han, Wei Yan and 2 more

Abstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Restoring Balance in Autoimmune Hepatitis.Cellular and molecular gastroenterology and hepatology · 2026
    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

12 authors.

Yu LeiDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Han WangDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Yu ChenDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Shuhui WangDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Zhipeng DuDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Zheng HuangDepartment of Pediatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Muru WangDepartment of Gastroenterology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, Henan, China.
Shangshu NieDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Ping HanDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Wei YanDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.
Mei LiuDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China. Electronic address: fliumei@126.com.
Dean TianDepartment of Gastroenterology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China; Hubei Key Laboratory of Hepato-Biliary-Pancreatic Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China. Electronic address: datian@tjh.tjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsAutoimmune hepatitis (AIH) is a chronic progressive inflammatory liver disease, with its incidence increasing continuously worldwide. The mechanisms underlying the regulation of immune tolerance in AIH remain largely unknown. This study investigated a novel regulatory pathway of regulatory T cell/T helper 17 (Treg/Th17) balance involving the ubiquitin-conjugating enzyme E2O (UBE2O) and underlying mechanisms.

methodsUBE2O expression was analyzed in patients and mice with AIH. In vivo UBE2O overexpression in a chronic AIH model and naïve CD4

resultsWe detected a reduction of UBE2O expression in livers of patients and mice with AIH. Low expression of UBE2O indicated severe liver inflammatory injury. Hepatic UBE2O overexpression experiments demonstrated that UBE2O alleviated hepatic injury, inflammation, and fibrosis, and restored Treg/Th17 balance in experimental AIH. Mechanistically, UBE2O was found to interact with and promote ubiquitination degradation of YBX1 at lysine 135 (K135), leading to the reduction of interleukin-6 transcription and secretion in hepatocytes, thus rewiring naïve CD4

conclusionsOur study revealed a previously unrecognized hepatocellular UBE2O/YBX1/interleukin-6 axis in AIH that primes hepatocytes to restore immune tolerance. Targeting UBE2O might provide a promising therapeutic target for AIH by linking posttranslational modification and hepatic immune tolerance.

Indexed as

Hepatitis, AutoimmuneHepatocytesImmune ToleranceInterleukin-6Ubiquitin-Conjugating EnzymesAnimalsCell DifferentiationDisease Models, AnimalFemaleHumansLiverMaleMiceMice, Inbred C57BLSignal TransductionTh17 CellsInterleukin-6Ubiquitin-Conjugating EnzymesAutoimmune Hepatitis (AIH)Immune ToleranceUbiquitin-Conjugating Enzyme E2O (UBE2O)Y-Box-Binding Protein 1 (YBX1)

Identifiers

PMID41780884
PMCPMC13196572

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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.