The Halkias lab studies the cellular and molecular signals that drive human immune development with a focus on understanding how early life host-microbe interactions influence adaptive immune responses to perinatal inflammatory disorders such as preterm birth. Early life is a critical time in immune development marked by rapid exposure to environmental antigens. Microbial colonization of mucosal tissues plays a key role in the development and education of the host immune system and influences the susceptibility to immune-mediated disease later in life. Infants born preterm are predisposed to prenatal immune activation and inflammation, critical risk factors underlying much of the pathophysiology in this vulnerable population. In utero infection is the most frequently identified cause of spontaneous preterm birth and fetal T cell activation is associated with severe neonatal disease, yet the signals that drive the activation, differentiation, and regulation of fetal adaptive immunity are not known. We utilize immune and microbial transcriptomics, high parameter flow and mass cytometry, and humanized mouse models to understand the cellular and molecular interactions that instruct human immune cells during this critical window of development.
June 1, 2019 - April 1, 2023 - Harnessing immune regulatory mechanisms to target the fetal inflammatory response in preterm birth , PI . Sponsor: Burroughs Wellcome Fund, Sponsor Award ID: 1019828
July 1, 2017 - June 30, 2022 - Intrauterine sex steroids and human fetal T cell development , Principal Investigator . Sponsor: NIH, Sponsor Award ID: K08AI128007
July 1, 2017 - June 30, 2022 - Intrauterine sex steroids and fetal T cell development. , PI . Sponsor: NIH/NIAID, Sponsor Award ID: 5 K08 AI128007 02