ArticleScientific reports2017
Defective thymic output in WAS patients is associated with abnormal actin organization.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Capsaicin for cardiometabolic syndrome: multitarget mechanisms and therapeutic potential.Frontiers in nutrition · 2026Review
- Comprehensive clinical and immunologic characterization of Wiskott-Aldrich syndrome in Iran: a 10-year cohort study.BMC immunology · 2025Article
- Trends in TREC values according to age and gender in Chinese children and their clinical applications.European journal of pediatrics · 2022Article
- Article
- TREC and KREC profiling as a representative of thymus and bone marrow output in patients with various inborn errors of immunity.Clinical and experimental immunology · 2020Article
- A novel disorder involving dyshematopoiesis, inflammation, and HLH due to aberrant CDC42 function.The Journal of experimental medicine · 2019Article
- Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects.Blood · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wiskott-Aldrich syndrome protein (WASp) is a key regulator of the actin cytoskeleton. Defective T - cell function is a major cause for immune deficiency in Wiskott-Aldrich syndrome (WAS) patients. T cells originate in the bone marrow and develop in the thymus, and then migrate to peripheral tissues. TCR excision circles (TRECs) present in thymic output cells stably, which is used as a molecular marker for thymic output. We found that CD8
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