Evidence map›Paper›PMID 41311054›Full record

ArticleImmunology2026

Preventing Differentiation Towards Primitive Macrophages in Stem Cells With Down Syndrome.

Koki Harada, Keiichi Ishihara, Sayaka Wakayama, Teruhiko Wakayama, Sae Yamamoto, Haruhiko Sago, Shun Shimohama, Satoshi Akiba, Florent Ginhoux, Kazuyuki Takata

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunology, 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

10 authors.

Koki HaradaJoint Research Laboratory, Division of Integrated Pharmaceutical Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Keiichi IshiharaLaboratory of Pathological Biochemistry, Division of Pathological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.ORCID 0000-0001-8748-7218
Sayaka WakayamaAdvanced Biotechnology Center, University of Yamanashi, Yamanashi, Japan.
Teruhiko WakayamaAdvanced Biotechnology Center, University of Yamanashi, Yamanashi, Japan.
Sae YamamotoLaboratory of Pathological Biochemistry, Division of Pathological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Haruhiko SagoSanno Birth Center, Minato-ku, Tokyo, Japan.
Shun ShimohamaDepartment of Neurology, Sapporo Medical University, School of Medicine, Sapporo, Japan.
Satoshi AkibaLaboratory of Pathological Biochemistry, Division of Pathological Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.
Florent GinhouxSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Kazuyuki TakataJoint Research Laboratory, Division of Integrated Pharmaceutical Sciences, Kyoto Pharmaceutical University, Kyoto, Japan.

Funding

Japan Society for the Promotion of Science 20H03569Japan Society for the Promotion of Science 22H04822Japan Society for the Promotion of Science 22K07033Kobayashi FoundationKyoto Pharmaceutical University Fund for Collaborative ResearchMEXT-Supported Program for the Strategic Research Foundation at Private UniversitiesShimizu Foundation for Immunology and NeuroscienceSmoking Research Foundation
6 · The paper itself

Abstract

Down syndrome (DS) is characterised by delayed brain development and intellectual disabilities. Brain macrophages originate from primitive macrophages that arise from mesodermal cells in the yolk sac and play a role in brain development. Previously, we showed a reduced number of brain macrophages in Ts1Cje foetuses, a murine model of DS. However, the mechanism underlying this reduction in Ts1Cje embryos remains unknown. First, in this study, we identified that the reduced brain macrophages in Ts1Cje foetuses were microglia. This study further reports the low production of primitive macrophages from Ts1Cje mouse embryonic stem cells (Ts1Cje-mESCs). Gene expression profiling in Ts1Cje-mESC-derived cells indicated the persistence of pluripotency, preference for endodermal differentiation, and suppression of mesodermal differentiation. Consistently, Ts1Cje-mESC-derived cells showed the disturbed expression of cytokine receptors and apoptosis, and a decreased number of primitive macrophages was confirmed in the Ts1Cje yolk sac. A human induced pluripotent stem cell line established from an individual with DS also showed lower primitive macrophage production relative to diploidized controls. Thus, our data indicate resistance to mesodermal differentiation and impaired production of primitive macrophages in DS, providing valuable insights into abnormalities in brain development associated with DS.

Indexed as

BrainCell DifferentiationDown SyndromeMacrophagesMouse Embryonic Stem CellsAnimalsCells, CulturedDisease Models, AnimalHumansInduced Pluripotent Stem CellsMiceMicrogliaYolk SacdifferentiationendodermmesodermmicrogliaRNA sequencing

Identifiers

PMID41311054
PMCPMC12867592

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.