I am a white, heterosexual, cisgender female and a first-generation college graduate who grew up in a farming community in Michigan. I earned my BS in Biology at Lake Superior State University and my PhD in Pharmacology and Toxicology at Michigan State University under the mentorship of Dr. Norbert Kaminski. Because of a dual career family I stayed in the Kaminski lab for my post-doc during which time I had two children. After my post-doc I moved with my family to the Dayton-Cincinnati area in Ohio and started a non-tenure faculty position at Wright State University while my husband joined a medical practice. I am currently an Associate Professor in the Department of Pharmacology & Toxicology within the Boonshoft School of Medicine at Wright State University. I am actively involved in SOT and Ohio Valley SOT regional chapter.
I have spent the majority of my research career studying antibody regulation and B cell function. My research has focused on evaluating the molecular mechanisms responsible for altered immunoglobulin (Ig) expression by aryl hydrocarbon receptor (AhR) ligands. We have identified the mouse 3’ Ig heavy chain regulatory region (3’IghRR) as a sensitive target of a diverse range of xenobiotics, including AhR ligands. Xenobiotic-induced modulation of 3’IghRR activity corresponds to altered Ig expression and antibody secretion. My laboratory has made significant progress in defining the molecular mechanisms responsible for altered 3’IghRR activation. We are currently focused on translating this mechanistic understanding to human Ig heavy chain gene (IGH) expression. These efforts have identified species differences and critical knowledge gaps that bridge the fields of human B-cell biology, AhR signaling, and toxicology. Our current efforts are focused on elucidating the effects of environmental stressors such as exogenous and endogenous AhR ligands on human antibody production and the potential impact of previously identified genetic polymorphisms within the human IGH gene on these effects. Since these polymorphisms have been associated with several antibody-related diseases, the overall goal of our research is the development of improved methods to better predict and model the impact of environmental and genetic differences in the pathophysiology of antibody-mediated diseases.