ArticleToxicological sciences : an official journal of the Society of Toxicology2026
In vitro characterization of the role of aryl hydrocarbon receptor and bisphenol A on IL-17A regulation in mouse and human CD4+ T cells.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The objective of this investigation was to determine whether direct addition of BPA to cultured primary mouse or human naïve CD4+ T cells promotes IL-17A production and Th17 cell differentiation and to assess the role of aryl hydrocarbon receptor (AHR) in promoting IL-17A regulation. Kinetic studies showed IL-17 concentrations peaked by day 4 post-activation in the mouse and on day 6 in human CD4+ T cells under Th17 polarizing and nonpolarizing conditions. AHR activation in murine CD4+ T cells by TCDD or FICZ promoted IL-17A and IL-22 secretion compared with vehicle controls under non-Th17 polarizing conditions. In contrast, AHR antagonism by CH223191 promoted IL-17 production in human CD4+ T cells while IL-22 secretion was reduced compared with controls. AHR activation by FICZ in human CD4+ T cells decreased IL-17 while increasing IL-22 secretion. Conversely, AHR antagonism in murine CD4+ T cells suppressed IL-17A and IL-22 responses. BPA treatment of CD4+ T cells from either species did not produce a significant increase in IL-17A-positive cells or increased IL-17 secretion, whereas FICZ and CH223191 treatment induced IL-17A increases under nonpolarizing and/or polarizing conditions in CD4+ T cells from mouse and human, respectively. These studies suggest that BPA treatment of mature, naïve CD4+ T cells from either species does not induce IL-17A or IL-22 secretion, whereas AHR activation inversely regulates IL-17A responses between species. These results confirm published results showing CD4+ T cells are refractory to BPA-mediated effects on IL-17, suggesting reported BPA effects in murine CD4+ T cells may be strain-dependent.
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