Year of Award

2011

Document Type

Thesis - Campus Access Only

Degree Type

Master of Science (MS)

Other Degree Name/Area of Focus

Microbiology, Immunology

Department or School/College

Division of Biological Sciences

Committee Chair

Scott Wetzel

Committee Co-chair

Stephen Lodmell

Commitee Members

David Shepherd, Kevan Roberts

Keywords

Atrazine, cAMP, Foxp3, phosphodiesterase, regulatory T cells

Abstract

Atrazine (ATR) is a selective pre- and post-emergence herbicide widely used for agricultural purposes as well as weed control in non-crop areas. Although banned from the European Union in 2006 due to potential environmental and health risks, this common environmental toxicant is heavily used in the United States. ATR is the most common groundwater contaminant in the U.S. and millions of Americans are exposed to it daily. ATR has been associated with immune dysfunction as well as other human health risks. The mechanism by which ATR suppresses the immune system has not been defined. It is known that ATR is a phosphodiesterase inhibitor, which causes intracellular accumulation of cAMP. Furthermore, ATR is classified as an endocrine disrupting compound that elevates estrogen levels by increasing aromatase activity of gonadal tissues. Both cAMP and estrogen have been implicated in altering immune function. We show that ATR causes the inhibition CD4+ T cell activation, proliferation, and effector cytokine production and that these suppressive effects can be, in part, attributed to an increase in regulatory T cells associated with ATR treatment. An increase in regulatory T cells has never been described in association with ATR exposure and could help to explain ATR-mediated immune dysfunction.

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© Copyright 2011 Lindsay Elizabeth Thueson