ArticleFrontiers of medicine2025
Recurrent eosinophilia with a novel homozygous ARPC1B mutation.
Article in Frontiers of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Arp2/3 complex controls the development of homeostatic microglia.EMBO reports · 2026Article
- Molecular analysis and immunological characterization of a founder mutation causing ARPC1B deficiency.Genes and immunity · 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
- Case Report: Sirolimus as management strategy for thrombocytopenia related to ARPC1B deficiency.Frontiers in immunology · 2026Article
- The c.64 + 2 T > A Founder Variant Hits Home: Report on 14 Patients Expands the Phenotypic Landscape of Inherited ARPC1B Deficiency - a Comparative Analysis.Clinical reviews in allergy & immunology · 2025Article
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10 authors.
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Abstract
Cytoskeletal network dysregulation is a pivotal determinant in various immunodeficiencies and autoinflammatory conditions. This report reviews the significance of actin remodeling in disease pathogenesis, focusing on the Arp2/3 complex and its regulatory subunit actin related protein 2/3 complex subunit 1B (ARPC1B). A spectrum of cellular dysfunctions associated with ARPC1B deficiency, impacting diverse immune cell types, is elucidated. The study presents a patient featuring recurrent and persistent eosinophilia attributed to homozygous ARPC1B mutation alongside concomitant compound heterozygous cystic fibrosis transmembrane conductance regulator (CFTR) gene mutations. We used ARPC1B antibody to stain the patient's peripheral blood lymphocytes and those of the control. The defect in the ARPC1B gene in the present patient caused absent/low expression by immunofluorescence microscopy. The intricate interplay between cytoskeletal defects and immunological manifestations underscores the complexity of disease phenotypes, warranting further exploration for targeted therapeutic strategies.
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