ArticleThe Journal of clinical investigation2019
Loss of ARPC1B impairs cytotoxic T lymphocyte maintenance and cytolytic activity.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Unveiling sex-based differences in Parkinson's disease: a comprehensive meta-analysis of transcriptomic studies.Biology of sex differences · 2022Pooled it
- Actin conformation dynamics precede force generation in cytotoxic T lymphocytes.Communications biology · 2026Article
- Characterisation of a Leaky Splice-Site Mutation Associated with Phenotypic Diversity in Two Unrelated Patients with ARPC1B Deficiency.Journal of clinical immunology · 2026Article
- Acute priming using elevated fluid viscosity recovers 'bioRxiv : the preprint server for biology · 2026Article
- Case Report: Sirolimus as management strategy for thrombocytopenia related to ARPC1B deficiency.Frontiers in immunology · 2026Article
- Branched actin networks mediate macrophage-dependent host-microbiota homeostasis.Science (New York, N.Y.) · 2025Article
- A microexon in Arp2 alters tissue-specific Arp2/3-generated actin structures.bioRxiv : the preprint server for biology · 2025Article
- Recurrent eosinophilia with a novel homozygous ARPC1B mutation.Frontiers of medicine · 2025Article
- The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025Review
- ARPC1B Promotes Clear Cell Renal Cell Carcinoma Progression via the Wnt/β-Catenin Signaling Pathway.Oncology research · 2025Article
- CK-666 and CK-869 differentially inhibit Arp2/3 iso-complexes.EMBO reports · 2024Article
- Oleate Promotes Triple-Negative Breast Cancer Cell Migration by Enhancing Filopodia Formation through a PLD/Cdc42-Dependent Pathway.International journal of molecular sciences · 2024Article
- High expression of ARPC1B correlates with immune infiltration and poor outcomes in glioblastoma.Biochemistry and biophysics reports · 2024Article
- 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
- Multi-omic Profiling Reveals Early Immunological Indicators for Identifying COVID-19 Progressors.bioRxiv : the preprint server for 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
- The pyrin inflammasome, a leading actor in pediatric autoinflammatory diseases.Frontiers in immunology · 2023Review
- Immunodeficiency with susceptibility to lymphoma with complex genotype affecting energy metabolism (Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
CD8 cytotoxic T lymphocytes (CTLs) rely on rapid reorganization of the branched F-actin network to drive the polarized secretion of lytic granules, initiating target cell death during the adaptive immune response. Branched F-actin is generated by the nucleation factor actin-related protein 2/3 (Arp2/3) complex. Patients with mutations in the actin-related protein complex 1B (ARPC1B) subunit of Arp2/3 show combined immunodeficiency, with symptoms of immune dysregulation, including recurrent viral infections and reduced CD8+ T cell count. Here, we show that loss of ARPC1B led to loss of CTL cytotoxicity, with the defect arising at 2 different levels. First, ARPC1B is required for lamellipodia formation, cell migration, and actin reorganization across the immune synapse. Second, we found that ARPC1B is indispensable for the maintenance of TCR, CD8, and GLUT1 membrane proteins at the plasma membrane of CTLs, as recycling via the retromer and WASH complexes was impaired in the absence of ARPC1B. Loss of TCR, CD8, and GLUT1 gave rise to defects in T cell signaling and proliferation upon antigen stimulation of ARPC1B-deficient CTLs, leading to a progressive loss of CD8+ T cells. This triggered an activation-induced immunodeficiency of CTL activity in ARPC1B-deficient patients, which could explain the susceptibility to severe and prolonged viral infections.
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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.