Evidence map›Paper›PMID 41429263›Full record

ArticleBiomedical journal2025

Anti-PD-L1 improves barrier function and reduces CD103

Jinli Huang, Yi Zhang, Qiuhong Li, Min Wang, Han Zhou, Hui Su, Xin Sun

Abstract read
In one paragraph

Article in Biomedical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

  1. Review
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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

7 authors.

Jinli HuangDepartment of Pediatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Yi ZhangDepartment of Pediatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Qiuhong LiDepartment of Pediatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Min WangDepartment of Pediatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Han ZhouDepartment of Pediatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Hui SuDepartment of Geriatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. Electronic address: Huisu2014@163.com.
Xin SunDepartment of Pediatrics, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. Electronic address: sunxin6@fmmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgrammed death ligand 1 (PD-L1) was found to play an important role in maintaining tolerance and immune balance, and its mechanism of action on asthma still needs to be further clarified. We aim to block PD-L1 in vivo to further clarify its potential role in the pathogenesis of asthma. MATERIAL AND

methodsIn a juvenile asthma model, PD-L1 blockers were used to inhibit the expression of PD-L1 in vivo. By evaluating parameters that reflect airway hyperresponsiveness, airway inflammation, tissue damage, intestinal barrier function, and microbiome changes in mice, the impact of PD-L1 blockade on various physiological and immune indicators in asthma models is fully revealed.

resultsPD-L1 blockade reduces leukocyte infiltration in the lungs, including eosinophils, decreased levels of IgE and IgG1, and restored Th1/Th2 imbalance by reducing IL-4, IL-13, and GATA-3 while increasing IFN-γ. In addition, PD-L1 blockade significantly decreased levels of IL-17A/F and increased IL-10. Histological analysis of the lungs showed that PD-L1 blockade attenuated airway inflammatory cell infiltration and mucus hyperproduction. Further testing showed that the intestinal barrier function was improved after PD-L1 blockade. Mechanistic studies revealed that PD-L1 blockade improved microbiota composition in the lungs and gut, increased Lactobacillus, SCFA, and reduced LPS. As well as induced the downregulation of CD103

conclusionsPD-L1 blockade alleviated asthmatic airway inflammation by modulating gut and lung microbiota, improving intestinal barrier function, increasing SCFA levels, reducing LPS and CD103

Indexed as

AsthmaMicrobiotaPD-1/PD-L1 signaling pathway

Identifiers

PMID41429263
PMCPMC13634089

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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.