ArticleJournal of immunology (Baltimore, Md. : 1950)2026
The paracrine factor myeloid derived growth factor regulates the inflammatory fate and motility of human induced pluripotent stem cell-derived neutrophils.
Article in Journal of immunology (Baltimore, Md. : 1950), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Neutrophils are necessary for host defense but also contribute to tissue damage. Understanding the molecular mechanisms that govern human neutrophil development and fate is critical for developing interventions for treating and preventing human disease. Human induced pluripotent stem cell (iPSC)-derived neutrophils (iNeutrophils) are genetically tractable and provide a robust source of neutrophils to dissect molecular regulation and for potential use in infusion therapies. Here, we show that deletion of the paracrine factor myeloid-derived growth factor (MYDGF) in human iPSCs results in the development of iNeutrophils with improved zymosan-induced reactive oxygen species generation and antimicrobial functions. MYDGF-deficient iNeutrophils showed improved transendothelial migration to microbes in organotypic models and motility in confined microchannels. We identify MYDGF as a new endogenous inhibitor of cytosolic calcium dynamics that suppresses neutrophil inflammatory activity. Our findings show that MYDGF mediates neutrophil-to-neutrophil communication during migration through a paracrine mechanism. Since MYDGF-deficient iNeutrophils show improved effector and antimicrobial function, these cells may improve future therapeutic use of iNeutrophils for infusion therapies. Finally, soluble MYDGF provides an attractive strategy to limit chronic neutrophil-mediated inflammation and tissue damage.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.