Evidence map›Paper›PMID 33557842›Full record

ArticleRespiratory research2021

GITRL on dendritic cells aggravates house dust mite-induced airway inflammation and airway hyperresponsiveness by modulating CD4

Yaping Wang, Kou Liao, Bo Liu, Chao Niu, Wenjing Zou, Lili Yang, Ting Wang, Daiyin Tian, Zhengxiu Luo, Jihong Dai and 6 more

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 21% of its field
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

7 citing papers in PubMed, 14 citations in OpenAlex.

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  6. Long-chain acyl-CoA synthetase 4-mediated mitochondrial fatty acid metabolism and dendritic cell antigen presentation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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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

16 authors at 3 institutions in 1 country.

Yaping WangDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Kou LiaoDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Bo LiuNational Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Children's Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Chao NiuDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Wenjing ZouDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Lili YangDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Ting WangDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Daiyin TianDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Zhengxiu LuoDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Jihong DaiDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Qubei LiDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Enmei LiuDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Caihui GongDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Zhou FuDepartment of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China.
Ying Li *Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China. liying321@yeah.net.
Fengxia Ding *Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, Yuzhong District, No. 136, Zhongshan 2nd Road, Chongqing, 400014, China. 482613@hospital.cqmu.edu.cn.
Chongqing Medical University · CNChina International Science and Technology Cooperation · CNChildren's Hospital of Chongqing Medical University · CN

Funding

National Natural Science Foundation of China 81800032
6 · The paper itself

Abstract

backgroundGlucocorticoid-induced tumor necrosis factor receptor family-related protein ligand (GITRL) plays an important role in tumors, autoimmunity and inflammation. However, GITRL is not known to modulate the pathogenesis of allergic asthma. In this study, we investigated whether regulating GITRL expressed on dendritic cells (DCs) can prevent asthma and to elucidate its mechanism of action.

methodsIn vivo, the role of GITRL in modulating house dust mite (HDM)-induced asthma was assessed in adeno-associated virus (AAV)-shGITRL mice. In vitro, the role of GITRL expression by DCs was evaluated in LV-shGITRL bone marrow dendritic cells (BMDCs) under HDM stimulation. And the direct effect of GITRL was observed by stimulating splenocytes with GITRL protein. The effect of regulating GITRL on CD4

resultsGITRL was significantly increased in HDM-challenged mice. In GITRL knockdown mice, allergen-induced airway inflammation, serum total IgE levels and airway hyperresponsiveness (AHR) were reduced. In vitro, GITRL expression on BMDCs was increased after HDM stimulation. Further, knocking down GITRL on DCs partially restored the balance of Th1/Th2 and Th17/Treg cells. Moreover, GITRL stimulation in vitro inhibited Treg cell differentiation and promoted Th2 and Th17 cell differentiation. Similarly, GITRL mRNA expression was increased in the peripheral blood from asthmatic children.

conclusionsThis study identified a novel role for GITRL expressed by DCs as a positive regulator of CD4

Indexed as

PyroglyphidaeAnimalsAsthmaCD4-Positive T-LymphocytesCell DifferentiationChildCoculture TechniquesDendritic CellsFemaleHumansMiceMice, Inbred C57BLRespiratory HypersensitivityTumor Necrosis FactorsTnfsf18 protein, mouseTumor Necrosis FactorsAsthmaDendritic cellsGITRLTh17/TregTh1/Th2

Identifiers

PMID33557842
PMCPMC7869253
OpenAlexW3126836861

What OpenQuestion holds

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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.