Evidence map›Paper›PMID 28094276›Full record

ArticleScientific reports2017

B7-H3 participates in the development of Asthma by augmentation of the inflammatory response independent of TLR2 pathway.

Wenjing Gu, Xinxing Zhang, Yongdong Yan, Yuqing Wang, Li Huang, Meijuan Wang, Xuejun Shao, Zhengrong Chen, Wei Ji

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. miRNAs as Modern Biomarkers in Asthma Therapy.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. 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

9 authors at 1 institution in 1 country.

Wenjing GuDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Xinxing ZhangDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Yongdong YanDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Yuqing WangDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Li HuangDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Meijuan WangDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Xuejun ShaoDepartment of Clinical laboratory, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Zhengrong ChenDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Wei JiDepartment of Respiration, Children's Hospital Affiliated to Soochow University, Suzhou 215003, China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B7-H3, a new member of the B7 superfamily, acts as both a T cell costimulator and coinhibitor. Recent studies identified B7-H3 plays a critical role in the development of asthma. But the definitive mechanism is not clear. In this study, we further report that B7-H3 participates in the development of OVA-induced asthma in a murine model. And study its mechanism through the vitro and vivo experiment. Exogenous administration of B7-H3 strongly amplified the inflammatory response and augmented proinflammatory cytokines in vitro and vivo. These B7-H3-associated proinflammatory effects were not dependent on TLR2 signaling, as airway inflammation, eosinophils infiltration and cytokins (IL-4, IL-5, IL-13 and IFN-gamma) augment were still amplified in TLR2-deficient mice after administrated recombinant mouse B7-H3. These results indicated an important role for B7-H3 in the development of Th1 and Th2 cells in a murine model of asthma and its proinflammatory effects are not dependent on TLR2 signaling.

Indexed as

AnimalsAsthmaB7 AntigensBronchoalveolar Lavage FluidCell ProliferationCytokinesDisease Models, AnimalFemaleGene DeletionHumansImmunoglobulin EInflammationLungMice, Inbred C57BLNF-kappa BOvalbuminB7 AntigensCd276 protein, mouseCytokinesImmunoglobulin ENF-kappa BOvalbuminToll-Like Receptor 2

Identifiers

PMID28094276
PMCPMC5240336
OpenAlexW2576805656

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.