Evidence map›Paper›PMID 39417697›Full record

ArticleImmunity, inflammation and disease2024

Bioinformatics analysis of G protein subunit gamma transduction protein 2-autophagy axis in CD11b+ dendritic cells as a potential regulator to skew airway neutrophilic inflammation in asthma endotypes.

Xiaoying Ji, Yaoliang Zhou, Shendong He, Hongda Chen, Xianming Zhang, Zhifeng Chen, Jinwen Cai

Abstract read
In one paragraph

Article in Immunity, inflammation and disease, 2024. 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

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

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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. Gngt2 promotes inflammatory dendritic cell programming through an ATG5-NF-κB signaling axis in neutrophilic asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Article
4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Xiaoying JiDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang City, Guizhou Province, China.
Yaoliang ZhouEmergency and Disaster Medical Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen City, Guangdong Province, China.
Shendong HeDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Xianhu District, Nanning, Guangxi, China.
Hongda ChenDepartment of Traditional Chinese Medicine, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen City, Guangdong Province, China.
Xianming ZhangDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang City, Guizhou Province, China.ORCID 0000-0002-7719-9527
Zhifeng ChenDepartment of Respiratory and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha City, Hunan Province, China.
Jinwen CaiDepartment of Respiratory and Critical Care Medicine, The Third Xiangya Hospital of Central South University, Changsha City, Hunan Province, China.

Funding

2022 Basic Research Plan of Guizhou Province (Natural Science Project) Qian Ke He foundation-ZK [2022] General 425National Natural Science Foundation of China 82160009
6 · The paper itself

Abstract

backgroundAsthma is a heterogeneous inflammatory disease with two main clinical endotypes: type 2 (T2) high and low asthma. The plasticity and autophagy in dendritic cells (DCs) influence T helper (Th)2 or Th17 differentiation to regulate asthma endotypes. Enhanced autophagy in DCs fosters Th2 differentiation in allergic environments, while reduced autophagy favors Th17 cell differentiation in sensitized and infected environments. Autophagy regulation in DCs involves interaction with various pathways like G protein-coupled receptor (GPCR), mammalian target of rapamycin (mTOR), or phosphoinositide 3-kinase (PI3K) pathway. However, specific molecules within DCs influencing asthma endotypes remain unclear.

methodsGene expression data series (GSE) 64896, 6858, 2276, and 55247 were obtained from gene expression omnibus (GEO) database. Differentially expressed genes (DEGs) between CD103+ and CD11b+ DCs after induction by ovalbumin (OVA) and lipopolysaccharide (LPS) were analyzed using GEO2R. DEGs were examined through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein interaction (PPI) analyses. The hub gene network was construct with STRING database and Cytoscape. Autophagy differences in DCs and the selected hub gene in GSE6858, GSE2276, and GSE55247 were evaluated using student t tests.

resultsOur analysis identified 635 upregulated and 360 downregulated genes in CD11b+ DCs, compared to CD103+ DCs. These DEGs were associated with "PI3K-AKT signaling pathway," "Ras signaling pathway," and so forth. Thirty-five hub genes were identified, in which G protein subunit gamma transduction protein 2 (Gngt2) in CD11b+ DCs exhibited a relatively specific increase in expression associated with autophagy defects under the induction environment similar to T2 low asthma model. No significant difference was found in lung Gngt2 expression between T2 high asthma model and control group.

conclusionOur analysis suggested Gngt2 acted as an adapter molecule that inhibited autophagy, promoting Th17-mediated airway inflammation via the GPCR pathway in a T2 low asthma mice model. Targeting this pathway provides new asthma treatment strategies in preclinical research.

Indexed as

AsthmaAutophagyCD11b AntigenComputational BiologyDendritic CellsAnimalsGene Expression ProfilingGTP-Binding Protein gamma SubunitsHumansInflammationMiceNeutrophilsSignal TransductionCD11b AntigenGTP-Binding Protein gamma Subunitsasthma phenotypeautophagydendritic cellsGngt2Th17Th2

Identifiers

PMID39417697
PMCPMC11484477

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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.