ArticleJournal of cell science2024
Neutrophil motility is regulated by both cell intrinsic and endothelial cell ARPC1B.
Article in Journal of cell science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Arp2/3 involvement in intercellular bridge membrane fluctuations and constriction during neural stem cell divisions.iScience · 2026Article
- The Arp2/3 complex controls the development of homeostatic microglia.EMBO reports · 2026Article
- The paracrine factor myeloid derived growth factor regulates the inflammatory fate and motility of human induced pluripotent stem cell-derived neutrophils.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Actin-related protein 2/3 complex subunit 1B promotes cervical cancer cell tumorigenesis in vitro and in vivo.American journal of cancer research · 2026Article
- GATA1-deficient human pluripotent stem cells generate neutrophils with improved antifungal immunity that is mediated by the integrin CD18.PLoS pathogens · 2025Article
- GATA1-deficient human pluripotent stem cells generate neutrophils with improved antifungal immunity that is mediated by the integrin CD18.bioRxiv : the preprint server for biology · 2024Article
- PTP1B phosphatase dampens iPSC-derived neutrophil motility and antimicrobial function.Journal of leukocyte biology · 2024Article
- Advancing chemokine research: the molecular function of CXCL8.The Journal of clinical investigation · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Neutrophil-directed motility is necessary for host defense, but its dysregulation can also cause collateral tissue damage. Actinopathies are monogenic disorders that affect the actin cytoskeleton and lead to immune dysregulation. Deficiency in ARPC1B, a component of the Arp2/3 complex, results in vascular neutrophilic inflammation; however, the mechanism remains unclear. Here, we generated human induced pluripotent stem cell (iPSC)-derived neutrophils (denoted iNeutrophils) that are deficient in ARPC1B and show impaired migration and a switch from forming pseudopodia to forming elongated filopodia. We show, using a blood vessel on a chip model, that primary human neutrophils have impaired movement across an endothelium deficient in APRC1B. We also show that the combined deficiency of ARPC1B in iNeutrophils and endothelium results in further reduction in neutrophil migration. Taken together, these results suggest that ARPC1B in endothelium is sufficient to drive neutrophil behavior. Furthermore, the findings provide support for using the iPSC system to understand human neutrophil biology and model disease in a genetically tractable system.
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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.