PhD Candidate – Started Fall 2013
Hometown: Escanaba, MI
Advisor/Lab: Joshua Mezrich
Research Interests:Investigating the effects of air pollution on the lung’s adaptive immune response. Specifically, we are interested in the AHR-dependent effects of air pollution on T-cell populations. Airborne pollution, aryl hydrocarbon receptor, T-cells, lung transplant rejection.
Northern Michigan University (2011-2013)
Bachelors in Zoology (2013)
I am a huge hockey fan! I enjoy watching the Badgers, other local teams, and my nephew play. I also enjoy watching basketball and football. I am a complete animal lover. I have three cats and a dog back home that I miss dearly and I have a chinchilla here that keeps me company along with a number of house plants that I’ve acquired. Being from the Upper Peninsula of Michigan, I love enjoying the outdoors and beautiful lakes both in Madison and back home in Escanaba.
Why I joined METC
As an undergraduate, I switched majors a lot and was quite unsure of what I wanted to do when I completed my degree. During the summer after my fourth year, I had the opportunity to participate in the IBS-SRP, a summer research program that allowed me to work with a graduate student of the METC program on an environmental toxicology project. From that experience, I became very interested in the effects of toxicants on both humans and the environment and wanted to pursue these interests at the graduate level. METC is an interdisciplinary center allowing for the students to have a variety of options for their graduate career which was a major reason I joined. Plus, having loved my experience in Madison, both the city and the people within the program, it was an easy choice to come back.
The Mezrich lab is interested in investigating the effects of air pollution on the lungs adaptive immune response. Specifically, we are interested in the possible mechanisms of AHR-dependent effects of air pollution on T-cell populations.
Airborne pollution is a known risk factor for environmentally induced airway diseases (EIADS) such as asthma, chronic bronchitis, emphysema, and interstitial fibrosis. Additionally, lung transplantation is the treatment of choice for a number of end stage pulmonary diseases including chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and cystic fibrosis. Clinically it has been observed that, while the one-year survival for lung grafts is better than 80%, half of these grafts ultimately succumb to Obliterative Bronchiolitis (OB) and its associated syndrome, BOS over the ensuing years. BOS, considered to be chronic rejection of lung allografts, is thought to be an autoimmune-driven process that is the consequence of increased Th17 differentiation and interleukin (IL)-17 in the lung leading to graft destruction. Based on these observations, our lab hypothesizes that EIADs, including BOS, are the consequence of the lung’s intimate relationship with the airborne environment. Because of this relationship, we predict that subtle differences in the chemical constituencies of airborne particulate matter (PM) have significant consequences for the normal immunology of this organ.
PM is composed of several different constituents, including both polar and nonpolar components. Our lab is interested in understanding the fraction of particulate matter than is responsible for enhancing Th17 differentiation that can lead to graft rejection. Previous data from our lab, suggests that the aryl hydrocarbon receptor is mediating the enhanced Th17 differentiation and therefore the increase in IL-17 observed after addition of particulate matter in vitro. First and foremost, it is essential that we understand what fraction of the particulate matter is activating the AHR and causing the observed effect. Additionally, Th17 cells can produce both IL-17 which is associated with an inflammation response in this context, and IL-22 which is generally protective. Our lab is interested in understanding the mechanism in which drives the production of either IL-17 or IL-22 by this population of cells. It is important to identify which fraction of PM is responsible for aggravating EIAD because it impossible to remediate all forms of atmospheric pollution; but if we can identify a particular fraction found in combustible sources, such as mixtures of PAHs, efforts at remediation or avoidance for patients at risk can be more directed. In addition understanding the specific components of AHR binding, translocation, and transcription that are important in these effects, and examining the role of the AHR in immune and non-immune cells that encounter inhaled PM, to allow future targeting for treatment.
- McIver, S.C., Kang, Y-A, DeVilbiss, A.W., O’Driscoll, C.A., et al. The exosome complex establishes a barricade to erythroid maturation. Blood 2014:124(14): 2285-2297.