ArticleFrontiers in immunology2012
Autoimmunity in wiskott-Aldrich syndrome: an unsolved enigma.
Article in Frontiers in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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.
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.
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Who cites it
74 citing papers in PubMed, 133 citations in OpenAlex.
- Genetic architecture differences between pediatric and adult-onset inflammatory bowel diseases in the Polish population.Scientific reports · 2016Trial
- B-cell reconstitution after lentiviral vector-mediated gene therapy in patients with Wiskott-Aldrich syndrome.The Journal of allergy and clinical immunology · 2015Trial
- Lentiviral hematopoietic stem cell gene therapy in patients with Wiskott-Aldrich syndrome.Science (New York, N.Y.) · 2013Trial
- The Intertwining Between Arthritis and Inborn Errors of Immunity.Journal of clinical medicine · 2026Review
- A Cohort Study of 38 Classic Wiskott-Aldrich Syndrome Cases with Six Novel Mutations.Journal of clinical immunology · 2026Article
- A Novel Autoimmune Presentation of Wiskott-Aldrich Syndrome: Type 1 Diabetes.Immunity, inflammation and disease · 2026Article
- Inflammatory bowel disease and renal disorders: from clinical associations to shared mechanisms and management strategies.Frontiers in immunology · 2026Review
- Advancements in gene therapy for Wiskott-Aldrich syndrome: from early trials to emerging approaches.International journal of hematology · 2026Review
- Wiskott-Aldrich syndrome: clinical, immunological, and genetic characterization of the first Moroccan cohort.Frontiers in pediatrics · 2026Article
- Hydrophobic complementarity-determining region 3 (CDR3) sequences elucidate the cardiotoxic effects of immune checkpoint inhibitors.Research square · 2025Article
- Review
- Monogenic inflammatory bowel disease: An unfolding enigma.World journal of clinical pediatrics · 2025Review
- Necrotizing fasciitis secondary to Wiskott-Aldrich Syndrome: a unique clinical presentation. Case report.Case reports in plastic surgery & hand surgery · 2025Article
- Tviblindi algorithm identifies branching developmental trajectories of human B-cell development and describes abnormalities in RAG-1 and WAS patients.European journal of immunology · 2024Article
- Inborn Error of WAS Presenting with SARS-CoV-2-Related Multisystem Inflammatory Syndrome in Children.Journal of clinical immunology · 2024Article
- Myelin oligodendrocyte glycoprotein antibody-associated disease as a novel presentation of central nervous system autoimmunity in a pediatric patient with Wiskott-Aldrich syndrome.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023Article
- Autoimmunity in Primary Immunodeficiencies (PID).Clinical reviews in allergy & immunology · 2023Review
- Clinical Features and Genetic Analysis of Taiwanese Primary Immunodeficiency Patients with Prolonged Diarrhea and Monogenetic Inflammatory Bowel Disease.Journal of clinical immunology · 2023Article
- Monogenic inflammatory bowel disease-genetic variants, functional mechanisms and personalised medicine in clinical practice.Human genetics · 2023Review
- Microbiome and Its Dysbiosis in Inborn Errors of Immunity.Pathogens (Basel, Switzerland) · 2023Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Wiskott-Aldrich Syndrome (WAS) is a severe X-linked Primary Immunodeficiency that affects 1-10 out of 1 million male individuals. WAS is caused by mutations in the WAS Protein (WASP) expressing gene that leads to the absent or reduced expression of the protein. WASP is a cytoplasmic protein that regulates the formation of actin filaments in hematopoietic cells. WASP deficiency causes many immune cell defects both in humans and in the WAS murine model, the Was(-/-) mouse. Both cellular and humoral immune defects in WAS patients contribute to the onset of severe clinical manifestations, in particular microthrombocytopenia, eczema, recurrent infections, and a high susceptibility to develop autoimmunity and malignancies. Autoimmune diseases affect from 22 to 72% of WAS patients and the most common manifestation is autoimmune hemolytic anemia, followed by vasculitis, arthritis, neutropenia, inflammatory bowel disease, and IgA nephropathy. Many groups have widely explored immune cell functionality in WAS partially explaining how cellular defects may lead to pathology. However, the mechanisms underlying the occurrence of autoimmune manifestations have not been clearly described yet. In the present review, we report the most recent progresses in the study of immune cell function in WAS that have started to unveil the mechanisms contributing to autoimmune complications in WAS patients.
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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.