AhR represses AID expression. (A) Relative mRNA expression of aicda (normalized to β actin) under LPS and LTD stimulation at 48 h in WT and AhR^−/− splenic B cells. n = 3. Mean ± SD is shown. (B) Western blot showing AID, AhR, and tubulin (Tub; loading control) expression under LTD 96-h stimulation of splenic B cells (left) and LD/LPS 48-h stimulation of LN B cells from WT and AhR^−/− mice. A representative of two to three experiments is shown. (C) cyp1a1 expression in WT B cells stimulated with LTD for 48 h and infected with empty retroviral vector (pMIG) in the presence of DMSO or TCDD. n = 3. Mean ± SD is shown. (D) aicda expression in WT B cells stimulated with LTD for 48 h and infected with pMIG in the presence of DMSO or TCDD. n = 3. Mean ± SD is shown. (E) Western blot showing AID and tubulin (loading control) expression at 48 h LTD stimulated WT B cells infected with pMIG or pMIG-AID in the presence of DMSO or TCDD. A representative of two experiments is shown. (F) Percent GFP⁺ in pMIG- or pMIG-AID–infected WT B cells stimulated for 72 h with LTD in the presence of DMSO or TCDD. n = 4. Mean ± SD is shown. (G) Percent IgA⁺ cells of GFP-expressing WT B cells 72 h after pMIG or pMIG-AID infection in the presence of DMSO or TCDD. n = 4. Mean ± SD is shown. (H) ChIP using anti-AhR antibody. Binding of AhR to intronic silencer region 2a of aicda or to a region 2 kb downstream in intron 1 was examined. DNA in ChIP samples was quantified by quantitative PCR and normalized to input (5%). n = 3. Mean ± SD is shown. *, P < 0.05; **, P < 0.005 (Student’s t test).