ArticleHaematologica2011
The Wiskott-Aldrich syndrome protein permits assembly of a focused immunological synapse enabling sustained T-cell receptor signaling.
Article in Haematologica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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
36 citing papers in PubMed, 64 citations in OpenAlex.
- IgE Production Beyond Classical T-Cell Help.Immune network · 2026Review
- Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.Nature reviews. Immunology · 2026Review
- Immunological synapse: structures, molecular mechanisms and therapeutic implications in disease.Signal transduction and targeted therapy · 2025Review
- Bioinformatics Approach to Investigating the Immuno-Inflammatory Mechanisms of Periodontitis in the Progression of Atherosclerosis.Current issues in molecular biology · 2025Article
- Article
- Explainable machine learning for profiling the immunological synapse and functional characterization of therapeutic antibodies.Nature communications · 2023Article
- Physiological lentiviral vectors for the generation of improved CAR-T cells.Molecular therapy oncolytics · 2022Article
- Genome editing for primary immunodeficiencies: A therapeutic perspective on Wiskott-Aldrich syndrome.Frontiers in immunology · 2022Review
- Ena/VASP Protein-Mediated Actin Polymerization Contributes to Naïve CD8Frontiers in immunology · 2022Article
- Molecular Tuning of Actin Dynamics in Leukocyte Migration as Revealed by Immune-Related Actinopathies.Frontiers in immunology · 2021Review
- Actin Dynamics at the T Cell Synapse as Revealed by Immune-Related Actinopathies.Frontiers in cell and developmental biology · 2021Review
- Wiskott-Aldrich Syndrome Protein: Roles in Signal Transduction in T Cells.Frontiers in cell and developmental biology · 2021Review
- The role of actin and myosin in antigen extraction by B lymphocytes.Seminars in cell & developmental biology · 2020Review
- Cytoskeletal tension actively sustains the migratory T-cell synaptic contact.The EMBO journal · 2020Article
- Higher Incidence of B Cell Malignancies in Primary Immunodeficiencies: A Combination of Intrinsic Genomic Instability and Exocytosis Defects at the Immunological Synapse.Frontiers in immunology · 2020Review
- Actin Cytoskeleton Straddling the Immunological Synapse between Cytotoxic Lymphocytes and Cancer Cells.Cells · 2019Review
- Interfacial actin protrusions mechanically enhance killing by cytotoxic T cells.Science immunology · 2019Article
- Clinical Manifestations and Pathophysiological Mechanisms of the Wiskott-Aldrich Syndrome.Journal of clinical immunology · 2018Review
- Signals Controlling Lytic Granule Polarization at the Cytotoxic Immune Synapse.Frontiers in immunology · 2018Review
- Wiskott-Aldrich syndrome protein: Emerging mechanisms in immunity.European journal of immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundT-cell activation relies on the assembly of the immunological synapse, a structure tightly regulated by the actin cytoskeleton. The precise role of the Wiskott-Aldrich syndrome protein, an actin cytoskeleton regulator, in linking immunological synapse structure to downstream signaling remains to be clarified. DESIGN AND
methodsTo address this point, CD4(+) T cells from patients with Wiskott-Aldrich syndrome were stimulated with antigen-presenting cells. The structure and dynamics of the immunological synapse were studied by confocal and video-microscopy.
resultsUpon stimulation by antigen-presenting cells, Wiskott-Aldrich syndrome protein-deficient T cells displayed reduced cytokine production and proliferation. Although Wiskott-Aldrich syndrome T cells formed conjugates with antigen-presenting cells at normal frequency and exhibited normal T-cell receptor down-regulation, they emitted actin-rich protrusions away from the immunological synapse area and their microtubule organizing center failed to polarize fully towards the center of the immunological synapse. In parallel, abnormally dispersed phosphotyrosine staining revealed unfocused synaptic signaling in Wiskott-Aldrich syndrome T cells. Time-lapse microscopy confirmed the anomalous morphology of Wiskott-Aldrich syndrome T-cell immunological synapses and showed erratic calcium mobilization at the single-cell level.
conclusionsTaken together, our data show that the Wiskott-Aldrich syndrome protein is required for the assembly of focused immunological synapse structures allowing optimal signal integration and sustained calcium signaling.
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.