Innate immune responses to infection at the maternal-fetal interface
A primary focus of the Abrahams lab is to investigate the function of innate immune pattern recognition receptors at the maternal-fetal interface in order to understand how gestational tissues respond to infection, and how these responses play a role in adverse pregnancy outcomes, such as preterm birth. A major focus has been on placental trophoblast responses to infectious components. Studies in the lab have found that the trophoblast and other gestation cells and tissues expresses Toll-like receptors (TLRs) and Nod-like receptors (NLRs) and these elicit a wide range of effects; ranging from specific antiviral/microbial responses and inflammation to apoptosis. Moreover, these varied responses towards infectious components are regulated by specific downstream signaling pathways.
Mechanisms of antiphospholipid antibody-induced pregnancy complications
Another major area of interest to the Abrahams lab is the impact antiphospholipid antibodies have on a woman's chance of reproductive success. Women with antiphospholipid syndrome are at risk for recurrent pregnancy loss, preterm labor and preeclampsia. While antiphospholipid antibodies are known to directly target the placenta and impact trophoblast function, the precise mechanisms involved are poorly understood. Studies in the lab are characterizing the mechanisms by which antiphospholipid antibodies alter trophoblast function. We are also using our in vitro model to test the efficacy of various therapeutic agents in order to determine better ways to prevent obstetrical problems in these patients.
The role of placental microparticles in the pathogenesis of preeclampsia
Normal pregnancy is associated with the presence of circulating placental microvesicles (MV) and increased shedding and altered immune activation are seen in patients with preeclampsia, suggesting that placental MV may play a role in the pathophysiology of this disease. Studies by the lab have compared the effect of placental-derived MV from normal and preeclamptic patients on peripheral blood immune cell activation. Moreover, we have found that placental-derived MV express high levels of the human endogenous retrovirus (HERV), syncytin-1, and have demonstrated a functional role for this protein through its interactions with immune cells.