Evidence map›Paper›PMID 41562076›Full record

ArticleFrontiers in immunology2025

IL-22-STAT3-CD155 axis in alveolar echinococcosis: a pivotal role in immune exhaustion and therapeutic potential.

Liang Li, Xue Zhang, Ning Yang, Hui Liu, Junlong Xue, Jin Chu, Guodong Lv, Tuerganaili Aji, Xiaojuan Bi, Renyong Lin

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. 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. 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

10 authors.

Liang Li *State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Xue Zhang *State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Ning Yang *State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Hui LiuState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Junlong XueState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Jin ChuState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Guodong LvState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Tuerganaili AjiDepartment of Hepatobiliary and Hydatid Diseases, Digestive and Vascular Surgery Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Xiaojuan BiState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Renyong LinState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medical Research Institute, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Alveolar echinococcosis (AE), a lethal zoonosis caused by Methods: Liver tissue samples from AE patients and Results: IL-22 expression was significantly upregulated in liver tissues from both AE patients and Conclusion: Our study demonstrates that the IL-22-STAT3-CD155 axis, mediated by macrophage-hepatocyte crosstalk, drives the establishment of an immune-exhaustive microenvironment during

Indexed as

EchinococcosisEchinococcosis, HepaticEchinococcus multilocularisInterleukinsSTAT3 Transcription FactorAnimalsDisease Models, AnimalFemaleHepatocytesHumansInterleukin-22LiverMacrophagesMaleMiceSignal TransductionInterleukin-22InterleukinsSTAT3 protein, humanSTAT3 Transcription FactorAlveolar echinococcosisCD155Echinococcus multilocularisInterleukin-22macrophage-hepatocyte crosstalkSTAT3 signaling

Identifiers

PMID41562076
PMCPMC12813123

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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.