期刊
SCIENTIFIC REPORTS
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep37988
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资金
- Wellcome Trust
- Research Council UK Fellowship
- Biotechnology and Biological Science Research Council [BB/H019634/1]
- King's Health Partners R&D Challenge Fund [R120505]
- Department of Health via the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award
- King's College London
- King's College Hospital NHS Foundation Trust
- MRC
- AUK Centre in Allergic Mechanisms of Asthma by the Medical Research Council
- Asthma UK
- Asthma UK [MRC-Asthma UK Centre] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BB/H019634/1] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [EP/C509463/1] Funding Source: researchfish
- Medical Research Council [G1000758] Funding Source: researchfish
- BBSRC [BB/H019634/1] Funding Source: UKRI
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, naive 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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