My lab seeks to determine how perturbation of the developing immune system influences the risk for autoimmune diseases across the life span. In adults, the vast majority of blood and immune cells, including those recruited at sites of infection, are constantly generated from blood, or hematopoietic, stem cells (HSCs) in the bone marrow. As a postdoctoral fellow, I discovered a unique population of HSCs that exist only during early life and are responsible for generating distinct subsets of fetal-derived immune cells that persist across the life span. Furthermore, I found that simulating an infection in a pregnant mouse during this critical window of immune development expanded both fetal-specific HSCs and the immune cells they generate. Now, using techniques in immunology and developmental, molecular, and stem cell biology, including fate-mapping models, our lab will investigate how maternal inflammation alters the establishment and function of these fetal-derived immune cells across the life span, including their ability to produce antibodies and other immune signaling molecules. We will also determine whether the generation of these fetal-derived immune cells is altered in animal models of autoimmune disorders—and whether maternal infection increases the severity of disease in adult offspring. This work will enhance our understanding of the developmental basis for autoimmune disease susceptibility and reveal new targets for the treatment or prevention of autoimmune diseases.