ArticleProceedings of the National Academy of Sciences of the United States of America1997
Correction of the X-linked immunodeficiency phenotype by transgenic expression of human Bruton tyrosine kinase under the control of the class II major histocompatibility complex Ea locus control region.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 39 citations in OpenAlex.
- Bruton's Tyrosine Kinase-Mediated Signaling in Myeloid Cells Is Required for Protective Innate Immunity During Pneumococcal Pneumonia.Frontiers in immunology · 2021Article
- Targeting Bruton's tyrosine kinase in B cell malignancies.Nature reviews. Cancer · 2014Review
- Article
- Development of an enhanced B-specific lentiviral vector expressing BTK: a tool for gene therapy of XLA.Gene therapy · 2008Article
- X-linked agammaglobulinemia.Clinical reviews in allergy & immunology · 2000Review
- Murine MHC class II locus control region drives expression of human beta-glucocerebrosidase in antigen presenting cells of transgenic mice.Gene therapy · 1999Article
- Severe B cell deficiency and disrupted splenic architecture in transgenic mice expressing the E41K mutated form of Bruton's tyrosine kinase.The EMBO journal · 1998Article
- Btk dosage determines sensitivity to B cell antigen receptor cross-linking.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bruton tyrosine kinase (Btk) is essential for the development of pre-B cells to mature B cell stages. Btk-deficient mice manifest an X-linked immunodeficiency (xid) defect characterized by a reduction of peripheral IgMlow IgDhigh B cells, a lack of peritoneal CD5+ B cells, low serum levels of IgM and IgG3, and impaired responses to T cell independent type II (TI-II) antigens. We have generated transgenic mice in which expression of the human Btk gene is driven by the murine class II major histocompatibility complex Ea gene locus control region, which provides gene expression from the pre-B cell stage onwards. When these transgenic mice were mated onto a Btk- background, correction of the xid B cell defects was observed: B cells differentiated to mature IgMlowIgDhigh stages, peritoneal CD5+ B cells were present, and serum Ig levels and in vivo responses to TI-II antigens were in the normal ranges. A comparable rescue by transgenic Btk expression was also observed in heterozygous Btk+/- female mice in those B-lineage cells that were Btk-deficient as a result of X chromosome inactivation. These findings indicate that the Btk- phenotype in the mouse can be corrected by expression of human Btk from the pre-B cell stage onwards.
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