Evidence map›Paper›PMID 31730616›Full record

ArticlePLoS biology2019

Type I interferon limits mast cell-mediated anaphylaxis by controlling secretory granule homeostasis.

Toshihiko Kobayashi, Shiho Shimabukuro-Demoto, Hidemitsu Tsutsui, Noriko Toyama-Sorimachi

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 35% 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, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. LRO biogenesis and function: what can we learn from mast cells?Frontiers in cell and developmental biology · 2025
    Review
  8. Autoantibodies to type I interferons in patients with systemic mastocytosis.The journal of allergy and clinical immunology. Global · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Anaphylaxis: Focus on Transcription Factor Activity.International journal of molecular sciences · 2021
    Review
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

Toshihiko KobayashiDepartment of Molecular Immunology and Inflammation, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo, Japan.ORCID 0000-0002-3238-1544
Shiho Shimabukuro-DemotoDepartment of Molecular Immunology and Inflammation, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo, Japan.
Hidemitsu TsutsuiDepartment of Molecular Immunology and Inflammation, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo, Japan.
Noriko Toyama-SorimachiDepartment of Molecular Immunology and Inflammation, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo, Japan.ORCID 0000-0003-3474-0456
National Center for Global Health and Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferon (IFN-I) is a family of multifunctional cytokines that modulate the innate and adaptive immunity and are used to treat mastocytosis. Although IFN-I is known to suppress mast cell function, including histamine release, the mechanisms behind its effects on mast cells have been poorly understood. We here investigated IFN-I's action on mast cells using interferon-α/β receptor subunit 1 (Ifnar1)-deficient mice, which lack a functional IFN-I receptor complex, and revealed that IFN-I in the steady state is critical for mast cell homeostasis, the disruption of which is centrally involved in systemic anaphylaxis. Ifnar1-deficient mice showed exacerbated systemic anaphylaxis after sensitization, which was associated with increased histamine in the circulation, even though the mast cell numbers and high affinity immunoglobulin E receptor (FcεRI) expression levels were similar between Ifnar1-deficient and wild-type (WT) mice. Ifnar1-deficient mast cells showed increased secretory granule synthesis and exocytosis, which probably involved the increased transcription of Tfeb. Signal transducer and activator of transcription 1(Stat1) and Stat2 were unexpectedly insufficient to mediate these IFN-I functions, and instead, Stat3 played a critical role in a redundant manner with Stat1. Our findings revealed a novel regulation mechanism of mast cell homeostasis, in which IFN-I controls lysosome-related organelle biogenesis.

Indexed as

AnaphylaxisAnimalsCells, CulturedHistamineHomeostasisInterferon Type IMast CellsMiceReceptor, Interferon alpha-betaSecretory VesiclesSignal TransductionSTAT1 Transcription FactorSTAT2 Transcription FactorSTAT3 Transcription FactorHistamineInterferon Type IReceptor, Interferon alpha-betaStat1 protein, mouseSTAT1 Transcription FactorStat2 protein, mouseSTAT2 Transcription FactorStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID31730616
PMCPMC6892554
OpenAlexW2986728113

What OpenQuestion holds

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LicenceCC BY
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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.