Aryl hydrocarbon receptor is required for optimal B‐cell proliferation

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.