ArticleFrontiers in immunology2018
Hypomorphic Mutations in the BCR Signalosome Lead to Selective Immunoglobulin M Deficiency and Impaired B-cell Homeostasis.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- AIM2 positively regulates B cell activation and function through the SNX9-PI3K-WASP axis.Cell death and differentiation · 2026Article
- Pediatric selective IgM deficiency: clinical features and a preliminary risk index for immunoglobulin replacement therapy.Immunologic research · 2025Article
- Selective IgM deficiency: evaluation of 75 patients according to different diagnostic criteria.Immunologic research · 2024Observational
- Selective IgM Deficiency: Evidence, Controversies, and Gaps.Diagnostics (Basel, Switzerland) · 2023Review
- Inborn errors of human B cell development, differentiation, and function.The Journal of experimental medicine · 2023Review
- A Novel BLNK Gene Mutation in a Four-Year-Old Child Who Presented with Late Onset of Severe Infections and High IgM Levels and Diagnosed and Followed as X-Linked Agammaglobulinemia for Two Years.Case reports in immunology · 2022Article
- The Possible Role of Bruton Tyrosine Kinase Inhibitors in the Treatment of COVID-19: A Review.Current therapeutic research, clinical and experimental · 2022Review
- Selective immunoglobulin M deficiency in a patient with celiac disease and recurrent pneumonia.Clinical case reports · 2021Article
- Complement Factor H Modulates Splenic B Cell Development and Limits Autoantibody Production.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B cell activation via the B cell receptor (BCR) signalosome involves participation of signaling molecules such as BTK and BLNK. Genetic defects in these molecules are known to impair B cell differentiation and subsequently lead to agammaglobulinemia. Here we identified novel mutations in BTK and BLNK in two unrelated patients that perturb the intrinsic B-cell receptor signaling pathway and lead to selective IgM deficiency, whereas production of other immunoglobulin isotypes and IgG antibody response remain intact. Currently it is unknown how BCR signaling strength affects mature B cell development in humans. Both patients show reduced levels of BCR signalosome phosphorylation as well as impaired BCR-dependent Ca
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