Evidence map›Paper›PMID 39040105›Full record

ArticleFrontiers in immunology2024

An early regulatory mechanism of hyperinflammation by restricting monocyte contribution.

Megumi Akiyama, Masashi Kanayama, Yoshihiro Umezawa, Toshikage Nagao, Yuta Izumi, Masahide Yamamoto, Toshiaki Ohteki

Abstract read
In one paragraph

Article in Frontiers in immunology, 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. Article
  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

7 authors.

Megumi Akiyama *Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Masashi Kanayama *Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Yoshihiro UmezawaDepartment of Hematology, Graduate School of Medical and Dental Sciences, TMDU, Tokyo, Japan.
Toshikage NagaoDepartment of Hematology, Graduate School of Medical and Dental Sciences, TMDU, Tokyo, Japan.
Yuta IzumiDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.
Masahide YamamotoDepartment of Hematology, Graduate School of Medical and Dental Sciences, TMDU, Tokyo, Japan.
Toshiaki OhtekiDepartment of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immune cells play a key role in inflammation as a source of pro-inflammatory cytokines. However, it remains unclear how innate immunity-mediated inflammation is fine-tuned to minimize tissue damage and assure the host's survival at the early phase of systemic inflammation. The results of this study with mouse models demonstrate that the supply of monocytes is restricted depending on the magnitude of inflammation. During the acute phase of severe inflammation, monocytes, but not neutrophils, were substantially reduced by apoptosis and the remaining monocytes were dysfunctional in the bone marrow. Monocyte-specific ablation of

Indexed as

CytokinesInflammationMonocytesAnimalsApoptosisCytokine Release SyndromeDisease Models, AnimalFemaleHumansImmunity, InnateMaleMiceMice, Inbred C57BLCytokinesapoptosisCRS - cytokine release syndromecytokineinflammationmonocyte

Identifiers

PMID39040105
PMCPMC11260625

What OpenQuestion holds

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LicenceCC BY
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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.