Funding outcome

Survival of the fetus through pregnancy depends on the maintenance of immune tolerance to the non-self antigens present in the fetus. The fetus has half of it's antigens originating from the mother and half from the father; the mother's immune system tries to reject the fetus because it sees the fetus as foreign to the mother's immune system. Therefore, the mother's immune system needs to be suppressed during the pregnancy in order to allow the fetus to survive. Multiple localized mechanisms in the placenta contribute to fetal evasion from the mother's immune rejection. Here, we propose that immature red blood cells (CD71+ erythroid cells) also contribute in a good pregnancy outcome. Our preliminary data shows that these cells are expanded during the pregnancy in the mother's blood, placenta and cord blood. Interestingly, these cells are absent in healthy adults and non-pregnant women. We have recently discovered that these cells have immunosuppressive properties (can suppress the immune cells). Therefore, in this proposal I will characterize the functionality of these cells by doing a wide range of experiments. In addition, I will deplete these cells in a pregnancy mouse model by administering antibody against a marker on the surface of immature red blood cells (CD71). I also will investigate the presence and functionality of similar cells in human cord blood, placenta and mother's peripheral blood. These studies will enable me to understand the role of these newly identified cells in human and mouse pregnancy. Thus, my study will reveal a previously unappreciated role for immature red blood cells (CD71 + erythroid cells) in pregnancy with potential application for manipulating them for a good pregnancy outcome.