Evidence map›Paper›PMID 40606633›Full record

ArticleFrontiers in cellular and infection microbiology2025

TIM4+macrophages suppress the proinflammatory response to maintain the chronic alveolar echinococcosis infection.

Liang Wang, Yumei Liu, Yuyu Ma, Xuan Zhou, Maidinaimu Aibibula, Xue Zhang, Hui Zhao, Jinping Zhou, Fengming Tian, Xiumin Ma

Abstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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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

10 authors.

Liang Wang *Institute of Medical Sciences of Xinjiang Medical University, Department of Medical Laboratory Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China.
Yumei Liu *Clinical Laboratory Center, Hospital of Traditional Chinese Medicine affiliated to Xinjiang Medical University, Urumqi, China.
Yuyu MaInstitute of Medical Sciences of Xinjiang Medical University, Department of Medical Laboratory Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China.
Xuan ZhouInstitute of Medical Sciences of Xinjiang Medical University, Department of Medical Laboratory Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China.
Maidinaimu AibibulaInstitute of Medical Sciences of Xinjiang Medical University, Department of Medical Laboratory Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China.
Xue ZhangState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Hui ZhaoState Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China.
Jinping ZhouInstitute of Medical Sciences of Xinjiang Medical University, Department of Medical Laboratory Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China.
Fengming TianInstitute of Medical Sciences of Xinjiang Medical University, Department of Medical Laboratory Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China.
Xiumin MaInstitute of Medical Sciences of Xinjiang Medical University, Department of Medical Laboratory Center, Tumor Hospital Affiliated to Xinjiang Medical University, Urumqi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Alveolar echinococcosis (AE), a severe zoonotic disease predominantly endemic to pastoral regions, is characterized by hepatic parasitic lesions caused by Methods: This study investigated the role of T-cell immunoglobulin and mucin domain-4 (TIMD4/Tim-4) in patients with hepatic AE. In total, 129 patients were enrolled from the First Affiliated Hospital of Xinjiang Medical University between 1 March 2018 and 1 March 2021. Histological, genetic, and serological tests were employed to evaluate Tim-4 and inflammatory cytokine expression. The liver immune microenvironment at the middle and late stages of mice infected with Results: Clinical analysis revealed the upregulation of Tim-4 within the hepatic lesions of patients with AE, with its expression spatially localized to macrophage-enriched regions and functionally linked to extracellular inflammatory modulation. Meanwhile, the liver tissues of the patients had characteristic pathological changes in the vesicles and progressive fibrotic remodeling, concurrent with a significant suppression of proinflammatory cytokine activity. Tim-4+ macrophages inhibited the release of proinflammatory cytokines at the middle and late stages of Conclusions: Tim-4 attenuated the predominant proinflammatory response, thereby facilitating immune evasion by

Indexed as

EchinococcosisEchinococcosis, HepaticMacrophagesAdultAnimalsCytokinesDisease Models, AnimalEchinococcus multilocularisFemaleHumansInflammationLiverLiver CirrhosisMaleMembrane ProteinsMiceCytokinesMembrane ProteinsTIMD4 protein, humanEchinococcus multilocularisimmunityliver fibrosismacrophageparasite infectionTim-4

Identifiers

PMID40606633
PMCPMC12213818

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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.