The research in my laboratory focuses on the cellular and molecular interactions between the pathogen Toxoplasma gondii and the host immune system. T. gondii is an intracellular parasite that infects ~35% of the human population worldwide. In healthy individuals, a robust immune response controls the acute infection and drives the parasite into a dormant state. The parasite persists, however, and reactivation can cause severe disease. The goal of our research is to define mechanisms by which T. gondii modulates host immunity during infection, in an effort to better understand the molecular basis for the development of disease. We are currently pursuing two areas of research: 1) T. gondii modulation of immune receptors: Macrophages and dendritic cells serve as sentinels of host defense, by initiating microbicidal activities and alerting other cells of the immune system to the presence of an infection. As a highly successful pathogen, however, T. gondii has evolved the ability to evade, modulate, or manipulate the activities of these cells in order to persist. We are particularly interested in mechanisms by which the parasite affects the expression of immune receptors and ligands on the surfaces of macrophages and dendritic cells, thereby impacting intercellular communication. We are working to define the parasite and host factors that govern these activities. 2) Innate immunity at the maternal-fetal interface: T. gondii is one of a small number of pathogens that can cross the placenta during pregnancy and cause congenital infection in the fetus, leading to neurological abnormalities and vision impairment. The response of placental cells to the parasite, however, is not well understood. In this line of research, we are investigating the activation of innate immune responses during T. gondii infection at the maternal-fetal interface to identify the pathways that contribute to parasite pathogenesis and host defense in the placenta.
3238 McGaugh Hall
3336 McGaugh Hall