ArticleFrontiers in immunology2023
Hemophilia A subjects with an intron-22 gene inversion mutation show CD4
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Deleterious variants cluster in the A3 domain of factor VIII in people with severe hemophilia A and inhibitors.Research and practice in thrombosis and haemostasis · 2025Article
- Prevalence and Clinical Correlation of Intron 22 Inversion in Hemophilia A in Northeast India.Cureus · 2025Article
- MHC class II presentation of FVIII-AnnexinA5 fusion proteins internalized by antigen presenting cells.Frontiers in immunology · 2025Article
- The self-reactive FVIII T cell repertoire in healthy individuals relies on a short set of epitopes and public clonotypes.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Background: Almost half of severe hemophilia A (HA) is caused by an intron 22 inversion mutation (Int22Inv), which disrupts the 26-exon Objectives: To test the hypothesis that (putative) intracellular synthesis of FVIII proteins encoded by inverted Patients/Methods: Peripheral blood mononuclear cells (PBMCs) from 30 severe or moderate HA subjects (17 with an Int22Inv mutation) were tested by ELISPOT assays to detect cytokine secretion in response to FVIII proteins and peptides and to map immunodominant T-cell epitopes. Potential immunogenicity of FVIII sequences encoded by the Results: Eight of the Int22Inv subjects showed robust cytokine secretion from PBMCs stimulated with FVIII proteins and/or peptides, consistent with earlier publications from the Conti-Fine group. Peptide ELISPOT assays identified immunogenic regions of FVIII. Specificity for sequences encoded within Conclusions: PBMCs from multiple subjects with an Int22Inv mutation, with and without a current FVIII inhibitor, responded to FVIII epitopes. Furthermore, the FVIII region encoded by the exon 22-23 junction sequence was not remarkably immunoreactive and is therefore unlikely to contain an immunodominant, promiscuous CD4
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Registered trials
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