The Effects of Estrogen in Atrazine-mediated Foxp3 Induction and Inhibition of Cd4+ T Effector Cells
Year: 2014
Type: dissertation
Abstract: Atrazine (ATR) is a chlorotriazine herbicide that is heavily used in agricultural areas. Atrazine was banned in Europe in 2006 but it is still used in the United States. It is also the most common drinking water contaminant in the United States. Atrazine has been linked to adverse health effects and displays immunotoxicity. It is a potent phosphodiesterase inhibitor and has been shown to induce aromatase activity leading to elevated estrogen levels. Previous studies demonstrated that in vitro atrazine exposure inhibits CD4+ T cell activation and proliferation and increases the frequency of Foxp3+ CD4+ T cells with more severe phenotypes in male-derived cells. The decreased proliferation and activation of CD4+ T cells was not replicable by pharmacologically increasing cAMP. This, along with the sex bias, suggested that ATR elevation of estrogen could mediate an increased severity in T cell proliferation and activation, specifically through GPER-1. We show that treatment with the GPER-1 agonist G-1 can mimic effects seen with low concentrations of ATR but blockade of GPER-1 with the antagonist G-36 does not alleviate ATR-mediated effects on CD4+ T cells. We also show that estrogen can synergize with ATR to further decrease CD4+ T cell proliferation and activation upon challenge with antigen. Overall, GPER-1 does not appear to be involved in the ATR mediated decrease in CD4+ T cell proliferation, activation, or increase in the frequency of Foxp3+ Tregs in vitro.
Source: The Mathematics Enthusiast
Author: Tiffany R. Emmons
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W789281886