The World Health Organization estimates that 10% of the burden of disease worldwide is due to problems that arise during pregnancy which compromise the health of mother and fetus. Genetic, endocrine, metabolic, and cardiovascular factors contribute to pregnancy complications, e.g spontaneous abortion, pre-eclampsia, fetal growth restriction, preterm labor and still birth. Some of these problems are due to placental dysfunction (1). Attaching to and invading deep into the specialized uterine mucosa called decidua, which is rich in maternal immune cells, the placenta is the fetus’s lifeline. It grows from the blastocyst-derived trophoblast and, once formed, nourishes the fetus trough the umbilical cord. Carrying genetic material from another individual (the father), the placenta ought to be targeted by the immune system that specializes in detecting and destroying what is different from self. Significant pathology, including allergy, autoimmunity, transplant rejection, and sepsis is caused by exaggerated, inappropriate, unwanted, or systemic immune responses. Do interactions between the placenta and maternal immune system influence pregnancy complications? And if we understand these interactions, can we intervene to improve pregnancy outcome?