Evidence map›Paper›PMID 31216735›Full record

ReviewInternational journal of molecular sciences2019

Potential Mechanisms of T Cell-Mediated and Eosinophil-Independent Bronchial Hyperresponsiveness.

Mayumi Saeki, Tomoe Nishimura, Noriko Kitamura, Takachika Hiroi, Akio Mori, Osamu Kaminuma

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Sophoraflavanone G fromInternational journal of molecular sciences · 2022
    Article
  5. Article
  6. The Role of CD4International journal of molecular sciences · 2021
    Review
  7. Article
  8. An update on the diagnostic biomarkers for asthma.Journal of family medicine and primary care · 2021
    Review
  9. Article
  10. Article
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

6 authors at 2 institutions in 1 country.

Mayumi SaekiAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan. saeki-my@igakuken.or.jp.
Tomoe NishimuraAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan. nishimura-tm@igakuken.or.jp.
Noriko KitamuraAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan. kitamura-nr@igakuken.or.jp.
Takachika HiroiAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan. hiroi-tk@igakuken.or.jp.
Akio MoriAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan. mori-kkr@umin.ac.jp.
Osamu KaminumaAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan. okami@hiroshima-u.ac.jp.ORCID 0000-0003-1211-0410
Tokyo Metropolitan Institute of Medical Science · JPHiroshima University · JP

Funding

Japan Society for the Promotion of Science 15K07787Japan Society for the Promotion of Science 26860122Nipponham Foundation N.A.Tojuro Iijima Foundation for Food Science and Technology N.A.
6 · The paper itself

Abstract

Bronchial asthma is a chronic disease characterized by reversible airway obstruction, mucus production, and bronchial hyperresponsiveness (BHR). Although Th2 cell-mediated eosinophilic inflammation is an important disease mechanism in the majority of patients with bronchial asthma, recent studies suggest the possible development of Th2-independent airway inflammation and BHR. These non-Th2 endotype patients seem to consist of multiple subgroups, and often do not respond to inhaled corticosteroids. Therefore, to understand the pathogenesis of asthma, it is important to characterize these non-Th2 subgroups. Recently, we demonstrated that Th9 cells induce eosinophil infiltration and eosinophil-independent BHR, and Th9 cells-mediated BHR may be resistant to glucocorticoid. In this review, we summarize the contribution of several T cell subsets in the development of bronchial asthma and introduce our recent study demonstrating Th9 cell-mediated and eosinophil-independent BHR.

Indexed as

AnimalsAsthmaBronchial HyperreactivityEosinophilsHumansTh17 CellsTh1 CellsTh2 CellsT-Lymphocyte Subsetsairway inflammationallergyasthmabronchial hyper responsiveness

Identifiers

PMID31216735
PMCPMC6627885
OpenAlexW2952147493

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.