Evidence map›Paper›PMID 41880492›Full record

ArticleScience advances2026

Pathogenic GM-CSF drives functional diversification of inflammatory macrophages in autoimmune arthritis.

Hiroki Mukoyama, Yusuke Takeuchi, Daiya Ohara, Yoonha Lee, Hitomi Watanabe, Hiroki Kato, Gen Kondoh, Akio Morinobu, Keiji Hirota

Abstract read
In one paragraph

Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Hiroki MukoyamaLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0000-0001-6871-5182
Yusuke TakeuchiLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0000-0003-2491-9524
Daiya OharaLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0009-0004-7946-6352
Yoonha LeeLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0009-0009-8098-9966
Hitomi WatanabeLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0000-0001-6448-9966
Hiroki KatoInstitute of Cardiovascular Immunology, Medical Faculty, University Hospital Bonn, University of Bonn, Bonn, Germany.ORCID 0000-0002-9571-4895
Gen KondohLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0000-0002-2564-0149
Akio MorinobuDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Keiji HirotaLaboratory of Integrative Biological Science, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0000-0002-4737-0661

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune T cells orchestrate joint inflammation and pain in concert with synovial macrophages; however, the mechanisms governing the development and functional diversification of these macrophages remain unclear. Using a model of T helper 17 cell (T

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesGranulocyte-Macrophage Colony-Stimulating FactorMacrophagesAnimalsCell DifferentiationCytokinesInflammationMiceSynovial MembraneTh17 CellsCytokinesGranulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID41880492
PMCPMC13015902

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.