| First Author | Villa M | Year | 2017 |
| Journal | EMBO J | Volume | 36 |
| Issue | 1 | Pages | 116-128 |
| PubMed ID | 27875245 | Mgi Jnum | J:239088 |
| Mgi Id | MGI:5824932 | Doi | 10.15252/embj.201695027 |
| Citation | Villa M, et al. (2017) Aryl hydrocarbon receptor is required for optimal B-cell proliferation. EMBO J 36(1):116-128 |
| abstractText | 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. |
