Evidence map›Paper›PMID 38540778›Full record

ArticleBiomolecules2024

CD69 Signaling in Eosinophils Induces IL-10 Production and Apoptosis via the Erk1/2 and JNK Pathways, Respectively.

Dan Van Bui, Linh Manh Nguyen, Akira Kanda, Hanh Hong Chu, Nhi Kieu Thi Le, Yasutaka Yun, Yoshiki Kobayashi, Kensuke Suzuki, Akitoshi Mitani, Akihiro Shimamura and 4 more

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

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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

14 authors at 2 institutions in 3 countries.

Dan Van BuiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.
Linh Manh NguyenDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0009-0001-6844-0366
Akira KandaDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0001-6324-721X
Hanh Hong ChuDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.
Nhi Kieu Thi LeDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.
Yasutaka YunDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0002-6879-6303
Yoshiki KobayashiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0003-3755-3074
Kensuke SuzukiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0003-1659-1549
Akitoshi MitaniDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0002-2062-5505
Akihiro ShimamuraDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.
Kenta FukuiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.
Shunsuke SawadaDentistry and Oral Surgery and Care Center, Kansai Medical University Hospital, Osaka 573-1010, Japan.ORCID 0000-0002-5856-5835
David DombrowiczUniversity of Lille, Inserm, CHU Lille, Institut Pasteur de Lille, 59000 Lille, France.ORCID 0000-0002-0485-8923
Hiroshi IwaiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Osaka 573-1010, Japan.ORCID 0000-0003-2646-8173
Kansai Medical University · JPInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionEosinophils contribute to the pathogenesis of allergic diseases, including asthma, allergic rhinitis, and atopic dermatitis. We previously reported that human tissue eosinophils have high CD69 expression compared to blood eosinophils, and its expression is correlated with disease severity and the number of infiltrated eosinophils. However, biological CD69 signaling activity in eosinophils remains unclear.

methodsCD69 expression on lung tissue eosinophils obtained from mice with ovalbumin-induced asthma was measured using flow cytometry. CD69 crosslinking was performed on eosinophils purified from the spleen of IL-5 transgenic mice to investigate CD69 signaling and its function in eosinophils. Then, qPCR, Western blot, enzyme-linked immunosorbent assay, and survival assay results were analyzed.

resultsSurface CD69 expression on lung tissue eosinophils in the asthma mice model was 2.91% ± 0.76%, whereas no expression was detected in the healthy group. CD69-expressed eosinophils intrinsically have an upregulation of IL-10 mRNA expression. Moreover, CD69 crosslinking induced further pronounced IL-10 production and apoptosis; these responses were mediated via the Erk1/2 and JNK pathways, respectively.

conclusionsOur results suggested that CD69

Indexed as

AsthmaEosinophilsAnimalsAntigens, CDApoptosisHumansInterleukin-10MAP Kinase Signaling SystemMiceAntigens, CDIL10 protein, mouseInterleukin-10asthmaCD69crosslinkingeosinophilErk1/2IL-10JNKsurvivaltype 2 inflammation

Identifiers

PMID38540778
PMCPMC10968075
OpenAlexW4392912172

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LicenceCC BY
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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.