My lab seeks to better understand why individuals in early life are more susceptible to infection than adults and respond poorly to vaccination. While the underlying basis for this increase in susceptibility is not known, many reports have indicated that it is due to quantitative and qualitative differences in neonatal T lymphocytes. We believe these differences arise from altered programs of T cell production and maintenance during early stages of development. In early life, there is a greater proportion of immature recent thymic emigrants, more extensive homeostatic proliferation of naïve T cells, different hematopoietic precursors, and a smaller repertoire of T cells. We are currently using neonatal mouse models of infectious diseases to determine the relative contribution of these differences toward impaired adaptive immune responses. The goal of my research is to identify the most critical primary defects in neonatal T cells, as well as to uncover the mechanisms that underlie such defects. Knowledge gained from these studies will then be used to design more effective therapeutic interventions and vaccines that can be safely administered in early life.