ArticleScientific reports2016
Global gene regulation during activation of immunoglobulin class switching in human B cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
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- Transcription Factor Bhlhe40 in Immunity and Autoimmunity.Trends in immunology · 2020Review
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- The Applicability of Mouse Models to the Study of Human Disease.Methods in molecular biology (Clifton, N.J.) · 2019Article
- The transcriptional response of mouse spleen B cells to IL-4: Comparison to the response of human peripheral blood B cells.Biochemistry and biophysics reports · 2018Article
- Alternative splicing: the pledge, the turn, and the prestige : The key role of alternative splicing in human biological systems.Human genetics · 2017Review
- Identification of sequence variants influencing immunoglobulin levels.Nature genetics · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Immunoglobulin class switch recombination (CSR) to IgE is a tightly regulated process central to atopic disease. To profile the B-cell transcriptional responses underlying the activation of the germinal centre activities leading to the generation of IgE, naïve human B-cells were stimulated with IL-4 and anti-CD40. Gene expression and alternative splicing were profiled over 12 days using the Affymetrix Human Exon 1.0 ST Array. A total of 1,399 genes, forming 13 temporal profiles were differentially expressed. CCL22 and CCL17 were dramatically induced but followed a temporal trajectory distinct from classical mediators of isotype switching. AICDA, NFIL3, IRF4, XBP1 and BATF3 shared a profile with several genes involved in innate immunity, but with no recognised role in CSR. A transcription factor BHLHE40 was identified at the core of this profile. B-cell activation was also accompanied by variation in exon retention affecting >200 genes including CCL17. The data indicate a circadian component and central roles for the Th2 chemokines CCL22 and CCL17 in the activation of CSR.
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Registered trials
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