Objective <p>Activation of the aryl hydrocarbon receptor (AhR) with its prototypical agonist 2,3,7,8-tetrachlorodibenzo-<i>p</i>-dioxin (TCDD) suppresses B cell class switch recombination (CSR). In T cells, AhR activation with structurally diverse agonists has been reported to alter differentiation non-uniformly with some agonists supporting Th17 development and others supporting Treg development. To determine if B cell CSR is similarly impacted by different AhR agonists, we exposed mouse splenic CD19⁺ cells to the AhR agonists, cinnabarinic acid (25 µM), 5,11-dihydroindolo[3,2-b]carbazole-6-carboxaldehyde (FICZ, 0.2 µM), indole-3-carbanol (I3C, 200 µM), L-kynurenine (25 µM), tamoxifen (10 µM), or TCDD (50 nM), or to the AhR antagonist CH-223191 (100 µM), under conditions to stimulate activation and class switch to IgA.</p> Results <p>Relative to control cells (10.8% IgA⁺), significantly decreased proportions of IgA⁺ cells were observed after exposure to cinnabarinic acid (4.5%), FICZ (2.5%), I3C (2.3%), kynurenine (4.4%), and TCDD (3.9%). In contrast, CH-223,191 significantly increased the proportion of IgA⁺ cells (16.2%). These results suggest that suppression of CSR is a common effect of AhR agonists in activated murine B cells.</p>