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Aryl hydrocarbon receptor is required for optimal B‐cell proliferation
Author(s) -
Villa Matteo,
Gialitakis Manolis,
Tolaini Mauro,
Ahlfors Helena,
Henderson Colin J,
Wolf C Roland,
Brink Robert,
Stockinger Brigitta
Publication year - 2016
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201695027
Subject(s) - mill , library science , art history , history , archaeology , computer science
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.