In vitro characterization of the role of aryl hydrocarbon receptor and bisphenol A on IL-17A regulation in mouse and human CD4+ T cells
Clicks: 7
ID: 324868
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
1.8
/100
7 views
3 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #89 of 125 articles by views in toxicological sciences : an official journal of the society of toxicology
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 125 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
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 non-polarizing conditions. AHR activation in murine CD4+ T cells by TCDD or FICZ promoted IL-17A and IL-22 secretion compared to 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 to 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, while FICZ and CH223191 treatment induced IL-17A increases under non-polarizing 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 do not induce IL-17A or IL-22 secretion while 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.
| Reference Key |
openalex_W7202389337
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Lance K. Blevins, Robert B. Crawford, Norbert E. Kaminski |
| Journal | toxicological sciences : an official journal of the society of toxicology |
| Year | 2026 |
| DOI |
10.1093/toxsci/kfag101
|
| URL | |
| Keywords | Keywords not found |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.