Investigating the Effects of Inflammation on Regulatory T cells at the Maternal-Fetal Interface

Chorioamnionitis defined as infection and/or inflammation of the fetal membranes, remains a leading cause of preterm birth (PTB), largely due to limitations of current diagnostics, which detect inflammation only after significant maternal and fetal tissue damage occurs. This highlights the need for preventive strategies to sustain the anti-inflammatory state at the maternal fetal interface (MFI) throughout pregnancy. 
Regulatory T cells (Tregs) are crucial to maintaining this anti-inflammatory state, as they are significantly enriched at the MFI in healthy pregnancies, and their depletion is associated with various pregnancy complications resulting in PTB. Leveraging an established mouse model of ascending chorioamnionitis, our lab has shown that in addition to being depleted, Tregs lose their ability to secrete anti-inflammatory cytokines such as IL-10 and TGF-b1.  Despite these insights, the exact mechanisms by which inflammation at the MFI impacts Tregs remain incompletely described
My research aims to determine the molecular and cellular mechanism by which inflammation at the MFI impacts the stability and function of Tregs, and how this, in turn, influences the phenotype of immune cells at this interface. By defining these mechanisms, we aim to identify potential pathways that can be targeted to sustain an anti-inflammatory state at the MFI and thus reduce the incidence of PTB.