Toxoplasma gondii is a major source of congenital disease worldwide, but the cellular and molecular factors associated with its vertical transmission are largely unknown. In humans, the placenta forms the key interface between the maternal and fetal compartments and forms the primary barrier that restricts the hematogenous spread of microorganisms. This dissertation describes both the identification of two mechanisms of placental syncytiotrophoblast resistance to T. gondii infection and a preliminary understanding of the CCL22 response induced by the Toxoplasma dense granule protein GRA28. Collectively, these findings provide new insights into (1) protective role of the syncytiotrophoblast during T. gondii infection, (2) interferon-gamma independent restriction of T. gondii growth, and (3) parasite-directed manipulation of the intercellular communication between the placenta and components of the maternal immune system
