Article in Allergy, asthma & immunology research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 41% 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
3 citing papers in PubMed, 4 citations in OpenAlex.
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 at 3 institutions in 1 country.
Shuyu Chen *Department of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China.ORCID https://orcid.org/0000-0002-8068-649X
Li Yu *Department of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China.ORCID https://orcid.org/0000-0001-5754-7072
Yao Deng *Department of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China.ORCID https://orcid.org/0000-0002-3741-1933
Yuanyuan Liu *Department of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China.ORCID https://orcid.org/0000-0003-3829-6006
Lingwei WangDepartment of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China.ORCID https://orcid.org/0000-0001-8889-5117
Difei LiDepartment of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China.ORCID https://orcid.org/0000-0002-5538-7164
Kai YangDepartment of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China.ORCID https://orcid.org/0000-0002-1982-4398
Shengming LiuDepartment of Pulmonary and Critical Care Medicine, First Affiliated Hospital of Jinan University, Guangzhou, China.ORCID https://orcid.org/0000-0003-0193-8300
Ailin TaoThe Second Affiliated Hospital, Guangdong Provincial Key Laboratory of Allergy & Clinical Immunology, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China. taoailin@gzhmu.edu.cn.ORCID https://orcid.org/0000-0002-0584-921X
Rongchang ChenDepartment of Pulmonary and Critical Care Medicine, Shenzhen Institute of Respiratory Diseases, Shenzhen Key Laboratory of Respiratory Diseases, The Second Clinical Medical College of Jinan University (Shenzhen People's Hospital), First Affiliated Hospital of Southern University of Science and Technology (Shenzhen People's Hospital), Shenzhen, China. chenrc@vip.163.com.ORCID https://orcid.org/0000-0002-2396-3702
Southern Medical University Shenzhen Hospital · CNFirst Affiliated Hospital of Jinan University · CNSecond Affiliated Hospital of Guangzhou Medical University · CN
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
purposeInterleukin (IL)-17A plays a critical role in the pathogenesis of allergic airway inflammation. Yet, the exact roles of IL-17A in asthma are still controversial. Thus, the aim of this study was to dissect the roles of IL-17A in toluene diisocyanate (TDI)-induced mixed granulocytic asthma and to assess the effects of neutralizing antibody in different effector phases on TDI-induced asthma.
methodsIL-17A functions in allergic airway inflammation were evaluated using mice deficient in IL-17A (
resultsTDI-induced mixed granulocytic airway inflammation was IL-17A-dependent because airway hyperreactivity, neutrophil and eosinophil infiltration, airway smooth muscle thickness, epithelium injury, dysfunctional T helper (Th) 2 and Th17 responses, granulocytic chemokine production and mucus overproduction were more markedly reduced in the
conclusionsOur data demonstrated that IL-17A was required for the initiation of TDI-induced asthma, but functioned as a negative regulator of established allergic inflammation, suggesting that early abrogation of IL-17A signaling, but not late IL-17A neutralization, may prevent the progression of TDI-induced asthma and could be used as a therapeutic strategy for severe asthmatics in clinical settings.
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.
Early IL-17A Prevention Rather Than Late IL-17A Neutralization Attenuates Toluene Diisocyanate-Induced Mixed Granulocytic Asthma. · full record | OpenQuestion