ArticleThe Journal of clinical investigation1999
Mutations in Igalpha (CD79a) result in a complete block in B-cell development.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
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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
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 223 citations in OpenAlex.
- Meta-analysis of global and high throughput public gene array data for robust vascular gene expression discovery in chronic rhinosinusitis: Implications in controlled release.Journal of controlled release : official journal of the Controlled Release Society · 2021Pooled it
- Building an Interleukin-10-Producing Identity: How B Cells Acquire Interleukin-10 Competence and How Plasma Cell Differentiation Consolidates This Program.Immunological reviews · 2026Review
- The life cycle of tertiary lymphoid structures in pancreatic cancer-a window of opportunity for immunotherapy.Frontiers in immunology · 2026Review
- Human genetic influences on early B cell development.Journal of human immunity · 2025Review
- Proteomic profiling of over 13,000 proteins across ten mouse tissues using multi-dimensional peptide pre-fractionation.Journal of proteomics · 2025Article
- Systemic deficits in lipid homeostasis promote aging-associated impairments in B cell progenitor development.GeroScience · 2025Article
- Metabolic rewiring controlled by HIF-1α tunes IgA-producing B-cell differentiation and intestinal inflammation.Cellular & molecular immunology · 2025Article
- Maternal Helminth Infection Causes Dysfunctional B Cell Development in Male Offspring.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Expanding the Clinical Phenotype with CD79A Mutation and Refractory Helicobacter Bilis Infection.Journal of clinical immunology · 2024Article
- B-cells absence in patients diagnosed as inborn errors of immunity: a registry-based study.Immunogenetics · 2024Article
- Fluoxetine Successfully Treats Intracranial Enterovirus E18 Infection in a Patient with CD79a Deficiency Arising from Segmental Uniparental Disomy of Chromosome 19.Journal of clinical immunology · 2024Article
- Development and validation of an immune-related gene prognostic index for lung adenocarcinoma.Journal of thoracic disease · 2023Article
- Inborn errors of human B cell development, differentiation, and function.The Journal of experimental medicine · 2023Review
- Biologically informed deep learning to query gene programs in single-cell atlases.Nature cell biology · 2023Article
- Single-cell transcriptome analysis reveals a cellular immune response in freshwater dark sleeper (Frontiers in physiology · 2023Article
- Mechanism of CD79A and CD79B Support for IgM+ B Cell Fitness through B Cell Receptor Surface Expression.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Preclinical Analysis of Candidate Anti-Human CD79 Therapeutic Antibodies Using a Humanized CD79 Mouse Model.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Whole-Transcriptome Profiling and circRNA-miRNA-mRNA Regulatory Networks in B-Cell Development.Frontiers in immunology · 2022Article
- Thousands of induced germline mutations affecting immune cells identified by automated meiotic mapping coupled with machine learning.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Beyond monogenetic rare variants: tackling the low rate of genetic diagnoses in predominantly antibody deficiency.Cellular & molecular immunology · 2021Review
8 more citing papers are in PubMed but not listed here.
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6 authors at 3 institutions in 2 countries.
Funding
Abstract
Mutations in Btk, mu heavy chain, or the surrogate light chain account for 85-90% of patients with early onset hypogammaglobulinemia and absent B cells. The nature of the defect in the remaining patients is unknown. We screened 25 such patients for mutations in genes encoding components of the pre-B-cell receptor (pre-BCR) complex. A 2-year-old girl was found to have a homozygous splice defect in Igalpha, a transmembrane protein that forms part of the Igalpha/Igbeta signal-transduction module of the pre-BCR. Studies in mice suggest that the Igbeta component of the pre-BCR influences V-DJ rearrangement before cell-surface expression of mu heavy chain. To determine whether Igalpha plays a similar role, we compared B-cell development in an Igalpha-deficient patient with that seen in a mu heavy chain-deficient patient. By immunofluorescence, both patients had a complete block in B-cell development at the pro-B to pre-B transition; both patients also had an equivalent number and diversity of rearranged V-DJ sequences. These results indicate that mutations in Igalpha can be a cause of agammaglobulinemia. Furthermore, they suggest that Igalpha does not play a critical role in B-cell development until it is expressed, along with mu heavy chain, as part of the pre-BCR.
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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.