Tissue-resident cells of the innate immune system are the first responders upon infection or tissue damage at mucosal barrier sites. We use a murine model of influenza virus infection to understand the specific roles of lung resident dendritic cells and innate lymphocytes in antiviral responses. We also work with a tissue-engineered lung model in which human respiratory tract myeloid cells are exposed to respiratory syncytial virus, with the goal of understanding differences in neonatal and adult immunity. Our newest project will explore mechanisms by which sepsis induced by Gram-positive bacteria leads to immunosuppression.

Females often experience increased morbidity upon influenza virus infection, as well as increased incidence and severity of autoimmune disease and asthma. A major focus of the lab is to understand sex differences in numbers and function of innate type 2 lymphocytes (ILC2s) in homeostasis and upon inflammation. We published that female mice harbor significantly greater numbers of lung ILC2s in homeostasis, and we would like to understand how this sex difference contributes to ILC2 responses during infection and inflammatory disease. Ongoing projects will dissect the molecular basis of the differential regulation of female and male ILC2s by inflammatory stimuli and sex hormones in a model of influenza virus infection. This project also will help us to understand the female predominance of autoimmune disease.

My Publications