Bio: I received my PhD in Microbiology and Immunology at the University of Arkansas for Medical Sciences in Little Rock, AR, US. I obtained postdoctoral training in immunotoxicology at Arkansas Children’s Research Institute (ACRI) in Little Rock, AR. I moved into a tenure-track Assistant Professor position in the Department of Pediatrics at ACRI in 2008 and was promoted to Associate Professor with Tenure in 2014. In 2021, I moved my laboratory to the Department of Pharmaceutical Sciences, College of Pharmacy at the University of New Mexico in Albuquerque, NM where I am a Professor. I also direct the Environmental Health Sciences Core Center, New Mexico Integrative Science Program Incorporating Research in Environmental Sciences (NM-INSPIRES). My current work is focused on the impact of environmental contaminants on immune cells that drive autoimmune responses.

Abstract: The industrial solvent and widespread environmental contaminant trichloroethylene has been linked to T cell-mediated hypersensitivity reactions and autoimmune disease in humans and in mouse models of autoimmune disease.  Despite numerous studies evaluating the immunotoxicity of TCE, how this chemical impairs tolerance (i.e., unresponsiveness) to self-antigens is not known. CD4+ T cells are the major drivers of autoimmune responses. Our lab hypothesizes that a key TCE metabolite directly activates CD4+ T cells through key molecular targets that permit survival of autoreactive CD4s and their subsequent expansion to promote autoimmune disease. Our findings have shown that TCE increases activated proinflammatory Th1-like cells and disturbs expression of checkpoint molecules, PD1 and FasL, which are important in promoting tolerance of self-reactive T cells. This talk will focus on our ongoing work in CD4 T cells and how TCE exposure enhances autoreactivity through aberrant expression of molecules that enforce tolerance.