ArticleFrontiers in immunology2021
Thymic Epithelial Cell Alterations and Defective Thymopoiesis Lead to Central and Peripheral Tolerance Perturbation in MHCII Deficiency.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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
6 citing papers in PubMed, 12 citations in OpenAlex.
- Morphometric analysis of the thymic epithelial cell network using integrated and orthogonal digital pathology approaches.Communications biology · 2026Article
- Clinical, immunological, treatment characteristics, and outcomes in 22 patients with major histocompatibility complex class II deficiency.Frontiers in immunology · 2026Article
- The Proteostasis of Thymic Stromal Cells in Health and Diseases.The protein journal · 2024Review
- Primary and secondary defects of the thymus.Immunological reviews · 2024Review
- Clinical, Immunological, and Genetic Findings in Iranian Patients with MHC-II Deficiency: Confirmation of c.162delG RFXANK Founder Mutation in the Iranian Population.Journal of clinical immunology · 2023Article
- Inborn errors of immunity associated with defects of thymic development.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2022Review
Corrections and comments
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Authors and funding
29 authors at 16 institutions in 7 countries.
Funding
Abstract
Major Histocompatibility Complex (MHC) class II (MHCII) deficiency (MHCII-D), also known as Bare Lymphocyte Syndrome (BLS), is a rare combined immunodeficiency due to mutations in genes regulating expression of MHCII molecules. MHCII deficiency results in impaired cellular and humoral immune responses, leading to severe infections and autoimmunity. Abnormal cross-talk with developing T cells due to the absence of MHCII expression likely leads to defects in thymic epithelial cells (TEC). However, the contribution of TEC alterations to the pathogenesis of this primary immunodeficiency has not been well characterized to date, in particular in regard to immune dysregulation. To this aim, we have performed an in-depth cellular and molecular characterization of TEC in this disease. We observed an overall perturbation of thymic structure and function in both MHCII
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Registered trials
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