Aryl hydrocarbon receptor is required for optimal B‐cell proliferation

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Abstract
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 in vitro BCR stimulation and in vivo 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.
Funding Information
  • Francis Crick Institute
  • Cancer Research UK (C4639/A10822)
  • Medical Research Council
  • Wellcome
  • Boehringer Ingelheim Fonds

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