Year of Award
Master of Science (MS)
Cellular, Molecular and Microbial Biology
Department or School/College
Division of Biological Sciences
Stephen Lodmell, David Shepherd
regulatory T cell, immunotoxicity
University of Montana
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.
Emmons, Tiffany, "THE EFFECTS OF ESTROGEN IN ATRAZINE-MEDIATED FOXP3 INDUCTION AND INHIBITION OF CD4+ T EFFECTOR CELLS" (2014). Graduate Student Theses, Dissertations, & Professional Papers. 4350.
© Copyright 2014 Tiffany Emmons