期刊
EMBO JOURNAL
卷 36, 期 1, 页码 116-128出版社
WILEY-BLACKWELL
DOI: 10.15252/embj.201695027
关键词
aryl hydrocarbon receptor; B cells; cyclin O; proliferation
资金
- Francis Crick Institute
- Cancer Research UK
- UK Medical Research Council
- Wellcome Trust
- Flow Cytometry facility and Sequencing Facility
- Boehringer Ingelheim Fonds PhD Fellowship
- Wellcome Investigator Grant
- Cancer Research Programme Grant [C4639/A10822]
- Cancer Research UK [22357, 10822] Funding Source: researchfish
- The Francis Crick Institute [10160, 10159] Funding Source: researchfish
The aryl hydrocarbon receptor (AhR), a transcription factor known for mediating xenobiotic toxicity, is expressed in B cells, which are known targets for environmental pollutants. However, it is unclear what the physiological functions of AhR in B cells are. We show here that expression of Ahr in B cells is up-regulated upon B-cell receptor (BCR) engagement and IL-4 treatment. Addition of a natural ligand of AhR, FICZ, induces AhR translocation to the nucleus and transcription of the AhR target gene Cyp1a1, showing that the AhR pathway is functional in B cells. AhR-deficient (Ahr(-/-)) B cells proliferate less than AhR-sufficient (Ahr(+/+)) cells following invitro BCR stimulation and invivo adoptive transfer models confirmed that Ahr(-/-) B cells are outcompeted by Ahr(+/+) cells. Transcriptome comparison of AhR-deficient and AhR-sufficient B cells identified cyclin O (Ccno), a direct target of AhR, as a top candidate affected by AhR deficiency.
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