ArticleGenes and immunity2009
Spontaneous mutation in the Cd79b gene leads to a block in B-lymphocyte development at the C' (early pre-B) stage.
Article in Genes and immunity, 2009. 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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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Characterization of JNJ-80948543 a novel CD79bxCD20xCD3 trispecific antibody for B-cell non-Hodgkin lymphoma.Haematologica · 2026Article
- B-cells absence in patients diagnosed as inborn errors of immunity: a registry-based study.Immunogenetics · 2024Article
- Organ-specific host differential gene expression analysis in systemic candidiasis: A systems biology approach.Microbial pathogenesis · 2022Article
- A transcriptional signature accurately identifies Aspergillus Infection across healthy and immunosuppressed states.Translational research : the journal of laboratory and clinical medicine · 2020Article
- Ovarian Cancer Stem Cells with High ROR1 Expression Serve as a New Prophylactic Vaccine for Ovarian Cancer.Journal of immunology research · 2019Article
- Crosstalk between B lymphocytes, microbiota and the intestinal epithelium governs immunity versus metabolism in the gut.Nature medicine · 2011Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
We discovered B-lymphocyte-deficient mice within a group of B10.A-CD45.1 mice, and established that this deficiency was a recessively inherited trait. Gene mapping and sequence analysis showed a mutation in the third exon of the Cd79b gene (c.224G>A) that leads to the generation of a stop codon (W75X) in the mutant mouse. Fluorescent-activated cell sorting analysis of bone marrow cells showed that the mutant mice did not express the CD79B antigen. To establish where the block in development happens, we analyzed CD43(pos)B220(pos) B-lymphocyte precursors present in the mutant mice and found that the fraction C' (corresponding to early pre-B lymphocytes) was absent in the mutant mouse, whereas fractions B and C showed a relative accumulation. As expected, we found no IgG or IgA in mutant mice. These results suggest that this CD79b-mutant strain may be a useful tool for immunological research in human immunodeficiencies.
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