Evidence map›Paper›PMID 42548584›Full record

ArticleFrontiers in immunology2026

CCL20-CCR6 axis mediates mucosal-associated invariant T-M2 macrophage crosstalk to drive immune dysregulation in liver cirrhosis.

Bochen Chen, Ruoling Li, Shuya Zhang, Yiting Lou, Shuo Zhang, Jiaheng Lou, Jingcheng Zhang, Chuyun Xu, Tao Jiang, Yuanlin Lv

Abstract read
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In one paragraph

Article in Frontiers in immunology, 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.

Bochen Chen *The First Affiliated Hospital of Zhejiang Chinese Medical University(Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Ruoling Li *Zhejiang Chinese Medical University School of Basic Medical Sciences, Hangzhou, China.
Shuya Zhang *Zhejiang Chinese Medical University School of Basic Medical Sciences, Hangzhou, China.
Yiting LouThe Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Shuo ZhangZhejiang Chinese Medical University School of Basic Medical Sciences, Hangzhou, China.
Jiaheng LouZhejiang Chinese Medical University School of Basic Medical Sciences, Hangzhou, China.
Jingcheng ZhangZhejiang Chinese Medical University School of Basic Medical Sciences, Hangzhou, China.
Chuyun XuThe First Affiliated Hospital of Zhejiang Chinese Medical University(Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Tao JiangZhejiang Chinese Medical University School of Basic Medical Sciences, Hangzhou, China.
Yuanlin LvZhejiang Chinese Medical University School of Basic Medical Sciences, Hangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Cirrhosis is the end-stage of chronic liver disease characterized by progressive hepatic fibrosis and persistent immune dysregulation, yet the mechanisms by which immune cell crosstalk drives disease progression remain poorly understood. Methods: In the present study, we integrated bulk and single-cell transcriptomic analyses with immunofluorescence validation to investigate the role of the CCL20-CCR6 axis in MAIT cells-macrophages interactions during cirrhosis progression. Results: We identified eight core cirrhosis-associated immune genes ( Discussion: Collectively, these findings support the CCL20-CCR6 axis as a key regulator of hepatic immune dysregulation and fibrotic progression in liver cirrhosis, highlighting its potential as both a biomarker of disease activity and a therapeutic target for cirrhosis intervention.

Indexed as

Chemokine CCL20Liver CirrhosisMacrophagesMucosal-Associated Invariant T CellsReceptors, CCR6AnimalsCell CommunicationHumansSignal TransductionCCL20 protein, humanCCR6 protein, humanChemokine CCL20Receptors, CCR6CCL20cirrhosisimmune dysregulationM2 macrophagesMAIT cellssingle-cell transcriptomics

Identifiers

PMID42548584
PMCPMC13429398

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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.