Evidence map›Paper›PMID 26752722›Full record

ArticlePloS one2016

Essential Contribution of CD4+ T Cells to Antigen-Induced Nasal Hyperresponsiveness in Experimental Allergic Rhinitis.

Tomoe Nishimura, Osamu Kaminuma, Mayumi Saeki, Noriko Kitamura, Kunie Matsuoka, Hiromichi Yonekawa, Akio Mori, Takachika Hiroi

RetractedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
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  11. Role of CD4International journal of molecular sciences · 2020
    Review
  12. Article
  13. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Tomoe NishimuraAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Osamu KaminumaAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Mayumi SaekiAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Noriko KitamuraAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Kunie MatsuokaMammalian Genetics Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Hiromichi YonekawaBasic Research Center, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Akio MoriClinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan.
Takachika HiroiAllergy and Immunology Project, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Tokyo Metropolitan Institute of Medical Science · JPNational Sagamihara Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nasal hyperresponsiveness (NHR) is a characteristic feature of allergic rhinitis (AR); however, the pathogenesis of NHR is not fully understood. In this study, during the establishment of an experimental AR model using ovalbumin-immunized and -challenged mice, augmentation of the sneezing reaction in response to nonspecific proteins as well as a chemical stimulant was detected. Whether NHR is independent of mast cells and eosinophils was determined by using mast cell- and eosinophil-deficient mice. NHR was suppressed by treatment with anti-CD4 antibody, suggesting the pivotal contribution of CD4+ T cells. Furthermore, antigen challenge to mice to which in vitro-differentiated Th1, Th2, and Th17 cells but not naïve CD4+ T cells had been adoptively transferred led to the development of equivalent NHR. Since antigen-specific IgE and IgG were not produced in these mice and since antigen-specific IgE-transgenic mice did not develop NHR even upon antigen challenge, humoral immunity would be dispensable for NHR. CD4+ T cells play a crucial role in the pathogenesis of AR via induction of NHR, independent of IgE-, mast cell-, and eosinophil-mediated responses.

Indexed as

AnimalsAntibodies, MonoclonalAntigensCD4-Positive T-LymphocytesEosinophilsFemaleImmunizationImmunoglobulin EMast CellsMice, Inbred BALB CNoseRespiratory HypersensitivityRhinitis, AllergicAntibodies, MonoclonalAntigensImmunoglobulin E

Identifiers

PMID26752722
PMCPMC4709066
OpenAlexW2238252677

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.