ArticleJournal of immunology (Baltimore, Md. : 1950)2011
The role of germline promoters and I exons in cytokine-induced gene-specific class switch recombination.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. 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, 11 citations in OpenAlex.
- sciCSR infers B cell state transition and predicts class-switch recombination dynamics using single-cell transcriptomic data.Nature methods · 2024Article
- Physiology of the read-write genome.The Journal of physiology · 2014Review
- Unique contribution of IRF-5-Ikaros axis to the B-cell IgG2a response.Genes and immunity · 2012Article
- Enhancement of antibody class-switch recombination by the cumulative activity of four separate elements.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Germline transcription precedes class switch recombination (CSR). The promoter regions and I exons of these germline transcripts include binding sites for activation- and cytokine-induced transcription factors, and the promoter regions/I exons are essential for CSR. Therefore, it is a strong hypothesis that the promoter/I exons regions are responsible for much of cytokine-regulated, gene-specific CSR. We tested this hypothesis by swapping the germline promoter and I exons for the murine γ1 and γ2a H chain genes in a transgene of the entire H chain C-region locus. We found that the promoter/I exon for γ1 germline transcripts can direct robust IL-4-induced recombination to the γ2a gene. In contrast, the promoter/I exon for the γ2a germline transcripts works poorly in the context of the γ1 H chain gene, resulting in expression of γ1 H chains that is <1% the wild-type level. Nevertheless, the small amount of recombination to the chimeric γ1 gene is induced by IFN-γ. These results suggest that cytokine regulation of CSR, but not the magnitude of CSR, is regulated by the promoter/I exons.
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