ArticleJournal of immunology (Baltimore, Md. : 1950)2017
Disruption of Thrombocyte and T Lymphocyte Development by a Mutation in
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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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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.
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Who cites it
48 citing papers in PubMed, 79 citations in OpenAlex.
- Article
- Comprehensive Profiling of T- and B-Cell Receptor Repertoires Demonstrates Impaired Developmental and Activation of Adaptive Immunity in DOCK8 Deficiency.Journal of clinical immunology · 2026Article
- The Arp2/3 complex is required for in situ haptotactic response of microglia to iC3b.EMBO reports · 2026Article
- Molecular analysis and immunological characterization of a founder mutation causing ARPC1B deficiency.Genes and immunity · 2026Article
- Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.Nature reviews. Immunology · 2026Review
- Case Report: Sirolimus as management strategy for thrombocytopenia related to ARPC1B deficiency.Frontiers in immunology · 2026Article
- Pathological IgE Production in Inborn Errors of Immunity and Beyond.Immunological reviews · 2025Review
- Regulation of actin cytoskeletal dynamics in T cell development and function.Frontiers in immunology · 2025Review
- Disruption of the moonlighting function of CTF18 in a patient with T-lymphopenia.Frontiers in immunology · 2025Article
- CK-666 and CK-869 differentially inhibit Arp2/3 iso-complexes.EMBO reports · 2024Article
- β-Actin G342D as a Cause of NK Cell Deficiency Impairing Lytic Synapse Termination.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- HIV-1 Mediated Cortical Actin Disruption Mirrors ARP2/3 Defects Found in Primary T Cell Immunodeficiencies.bioRxiv : the preprint server for biology · 2024Article
- Hem1 inborn errors of immunity: waving goodbye to coordinated immunity in mice and humans.Frontiers in immunology · 2024Review
- A History and Atlas of the Human CD4Biomedicines · 2023Review
- ARPC5 deficiency leads to severe early-onset systemic inflammation and mortality.Disease models & mechanisms · 2023Article
- Inherited ARPC5 mutations cause an actinopathy impairing cell motility and disrupting cytokine signaling.Nature communications · 2023Article
- Branching out in different directions: Emerging cellular functions for the Arp2/3 complex and WASP-family actin nucleation factors.European journal of cell biology · 2023Article
- Is Your Kid Actin Out? A Series of Six Patients With Inherited Actin-Related Protein 2/3 Complex Subunit 1B Deficiency and Review of the Literature.The journal of allergy and clinical immunology. In practice · 2023Review
- Zebrafish: A Relevant Genetic Model for Human Primary Immunodeficiency (PID) Disorders?International journal of molecular sciences · 2023Review
- ARPC1B is a novel prognostic biomarker for kidney renal clear cell carcinoma and correlates with immune infiltration.Frontiers in molecular biosciences · 2023Article
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
Abstract
Regulation of the actin cytoskeleton is crucial for normal development and function of the immune system, as evidenced by the severe immune abnormalities exhibited by patients bearing inactivating mutations in the Wiskott-Aldrich syndrome protein (WASP), a key regulator of actin dynamics. WASP exerts its effects on actin dynamics through a multisubunit complex termed Arp2/3. Despite the critical role played by Arp2/3 as an effector of WASP-mediated control over actin polymerization, mutations in protein components of the Arp2/3 complex had not previously been identified as a cause of immunodeficiency. Here, we describe two brothers with hematopoietic and immunologic symptoms reminiscent of Wiskott-Aldrich syndrome (WAS). However, these patients lacked mutations in any of the genes previously associated with WAS. Whole-exome sequencing revealed a homozygous 2 bp deletion, n.c.G623DEL-TC (p.V208VfsX20), in Arp2/3 complex component
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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.