Evidence map›Paper›PMID 41777639›Full record

ArticleResearch and practice in thrombosis and haemostasis2026

Induced pluripotent stem cell-derived platelets kill multidrug-resistant

Qirui Lin, Kimiko Nonomura, Ieva Stirblyte, Sou Nakamura, Satoshi Uchiyama, Masaya Yamaguchi, Shigetada Kawabata, Miki Nagao, Katsue Suzuki-Inoue, Victor Nizet and 2 more

Abstract read
In one paragraph

Article in Research and practice in thrombosis and haemostasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Qirui LinDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Kimiko NonomuraDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Ieva StirblyteDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Sou NakamuraDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Satoshi UchiyamaDivision of Host-Microbe Systems and Therapeutics, Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, California, USA.
Masaya YamaguchiLaboratory of Microbial Informatics, Microbial Research Center for Health and Medicine, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka, Japan.
Shigetada KawabataDepartment of Microbiology, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Miki NagaoDepartment of Clinical Laboratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Katsue Suzuki-InoueDepartment of Clinical and Laboratory Medicine, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.
Victor NizetDivision of Host-Microbe Systems and Therapeutics, Department of Pediatrics, School of Medicine, University of California, San Diego, La Jolla, California, USA.
Koji EtoDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.
Naoshi SugimotoDepartment of Clinical Application, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Severe infection caused by multidrug-resistant bacteria, such as multidrug-resistant Objectives: We aimed to verify whether iPSC-PLTs are capable of killing MRSA and further elucidate the mechanisms involved in this process. Methods: We performed Results: All 3 iPSC-PLT clones demonstrated MRSA-killing capacity. Although only minimal activation of iPSC-PLTs was observed, antiplatelet agents inhibited this killing. Notably, plasma components enhanced the bactericidal activity of iPSC-PLTs, in part via immunoglobulin G, as evidenced by inhibition with an FcγRIIA-blocking antibody. Compared with wild-type MRSA, α-toxin-deficient strains were more susceptible to iPSC-PLT-mediated killing, suggesting that α-toxin acts as a suppressor of this platelet function. Furthermore, MyD88-deficient iPSC-PLTs exhibited impaired MRSA-killing capacity, indicating the indispensable role of Toll-like receptor 2-mediated signaling in this response. Conclusion: Collectively, our findings highlight the direct antimicrobial potential of iPSC-PLTs and provide mechanistic insights, particularly into the contribution of the Toll-like receptor-MyD88 axis. This study provided a basis for applying iPSC-PLTs as a novel therapeutic modality for combating MRSA infections and a genetically modifiable platform for investigating unknown platelet function within the context of antimicrobial immunity.

Indexed as

gene editingimmunoglobulin Ginduced pluripotent stem cellsMRSAMyD88plateletsStaphylococcal alpha-toxin

Identifiers

PMID41777639
PMCPMC12950430

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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.