Evidence map›Paper›PMID 39496822›Full record

ArticleScientific reports2024

IL-10 promotes Th17 cell differentiation by enhancing STAT1-dependent IL-6 production via IgE-stimulated mast cells.

Takafumi Numata, Masashi Ikutani, Ken Arae, Tatsukuni Ohno, Koki Okada, Takayuki Yoshimoto, Katsuko Sudo, Hajime Suto, Ko Okumura, Hirohisa Saito and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. 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
–field-weighted citation impact
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.

  1. Mast Cells in the Developing Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  2. Article
  3. 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

12 authors.

Takafumi NumataDepartment of Dermatology, Tokyo Medical University, Tokyo, 160-0023, Japan.
Masashi IkutaniGraduate School of Integrated Sciences for Life, Hiroshima University, 1-4-4 Kagamiyama, Higashi-Hiroshima, Hiroshima, 739-8528, Japan. mikutani@hiroshima-u.ac.jp.
Ken AraeDepartment of Immunology, Faculty of Health Sciences, Kyorin University, Tokyo, 181-8612, Japan.
Tatsukuni OhnoOral Health Science Center, Tokyo Dental College, Tokyo, 101-0061, Japan.
Koki OkadaGraduate School of Integrated Sciences for Life, Hiroshima University, 1-4-4 Kagamiyama, Higashi-Hiroshima, Hiroshima, 739-8528, Japan.
Takayuki YoshimotoDepartment of Immunoregulation, Institute of Medical Science, Tokyo Medical University, Tokyo, 160-8402, Japan.
Katsuko SudoPreclinical Research Center, Tokyo Medical University, Tokyo, 160-8402, Japan.
Hajime SutoAtopy Research Center, Juntendo University School of Medicine, Tokyo, 113-8412, Japan.
Ko OkumuraAtopy Research Center, Juntendo University School of Medicine, Tokyo, 113-8412, Japan.
Hirohisa SaitoDepartment of Allergy and Clinical Immunology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
Kazutoshi HaradaDepartment of Dermatology, Tokyo Medical University, Tokyo, 160-0023, Japan.
Susumu NakaeGraduate School of Integrated Sciences for Life, Hiroshima University, 1-4-4 Kagamiyama, Higashi-Hiroshima, Hiroshima, 739-8528, Japan. snakae@hiroshima-u.ac.jp.

Funding

Japan Society for the Promotion of Science 18H02847Japan Society for the Promotion of Science 22K08439Japan Society for the Promotion of Science 23K07795Japan Society for the Promotion of Science 24K11583National Institute of Biomedical Innovation ID 05-24
6 · The paper itself

Abstract

Mast cells (MCs) are tissue-resident cells of hematopoietic origin that play an important role in host's defense mechanism against nematodes. However, excessive activation of these cells contributes to the development of certain allergic diseases. Immunoglobin E (IgE) is one of the well-known molecules that activate MCs. Even in the absence of specific antigens, the binding of highly cytokinergic IgE to FcεRI on MCs prolongs their survival and induces cytokine production without enhancing their degranulation. In the present study, we examined the effects of the members of the interleukin-10 (IL-10) family of cytokines on IgE-mediated MCs functions. The receptors including Il10r1, Il10r2, and Il20r2, but not Il20r1, Il22r1 or Il28r1, were constitutively expressed in mouse bone marrow cell-derived cultured MCs (BMCMCs), suggesting that IL-10 may influence MCs function. Indeed, we found that only IL-10 could influence upon BMCMCs function; IL-10 enhanced prolongation of survival, promoted IL-6 and/or IL-13 production dependently of STAT1 and STAT3, and suppressed tumor necrosis factor production independently of STAT1 and STAT3 on IgE-stimulated BMCMCs. Moreover, the IL-10-mediated enhancement of IL-6 production by IgE-stimulated BMCMCs promotes Th17 cell expansion. These results suggest that IL-10 has a dual role as an anti-inflammatory and pro-inflammatory cytokine in MCs functions.

Indexed as

Cell DifferentiationImmunoglobulin EInterleukin-10Interleukin-6Mast CellsSTAT1 Transcription FactorTh17 CellsAnimalsCells, CulturedMiceSTAT3 Transcription FactorIL10 protein, mouseImmunoglobulin EInterleukin-10Interleukin-6Stat1 protein, mouseSTAT1 Transcription FactorSTAT3 Transcription FactorIL-10Mast cellsSTAT1STAT3Th17 cells

Identifiers

PMID39496822
PMCPMC11535472

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Registered trials

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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.