T cells respond to diverse inflammatory and infectious challenges. A major focus of our research is to understand how T cells regulate, and are regulated by, inflammation and infection and how this influences the balance between tissue repair and disease.
Local changes in metabolism that occur during injury, such as limiting oxygen availability (i.e. hypoxia), influences the host response and alters the outcome of injury. By studying these processes during mucosal models of inflammation, my research has shown that hypoxia triggers a negative feedback in T cells, to limit inflammation through enhanced regulatory T cell function. I have further extended these studies to demonstrate cross-talk between the generation of extracellular adenosine and inhibitory T cell functions. These studies have revealed the importance of microenvironmental signals in influencing T cell function and identified new potential avenues for therapeutic enhancement or intervention to modulate T cells.
We also focus on effector T cell function in the context of viral infection, seeking to gain new high-dimensional insight into the regulation of T cells. These studies have revealed IL-10 dependent regulation of effector T cell function as well as a prominent population of IL-10 expressing effector CD4 T cells elicited during primary infection. Ongoing studies seek to determine how IL-10 regulates effector CD4 T cell function and how IL-10 expression is coordinated with other cytokine expression during virus infection.