When a pregnant mother is exposed to infectious bacteria, her immune system kicks into gear and attacks the fetus, which can lead to fetal loss, stillbirth and premature birth— complications for which there is no therapy available today. 

But now, researchers have discovered the specific protein that sets off this process, and they say their findings may lay the groundwork for a potential treatment to preemptively and retroactively treat these abnormalities.

“What we know is that during pregnancy, the mother needs to be tolerant to the fetus so that it doesn’t reject the fetus like it would reject any other transplanted organ— and that tolerance is very intricately regulated, and has many moving parts that we’re only beginning to understand and appreciate. One of the most important aspects of that tolerance is preventing the harmful maternal immune cells from attacking the placenta,” lead study author Sing Sing Way, an infectious disease pediatrician at Cincinnati Children’s Hospital, told FoxNews.com.

According to the Centers for Disease Control and Prevention (CDC), one out of every nine infants in the U.S. was born premature— or before 37 weeks of a full pregnancy— in 2012, the most recent data available. Preterm birth in 2010 accounted for 35 percent of all infant deaths, which is more than any other cause, and the condition is also the top cause of long-term neurological disabilities in children. In 2006, the most recent CDC data available, about 25,970 stillbirths were reported. Stillbirths can occur after 20 weeks of gestation.

In their study, published Monday in the Journal of Clinical Investigation, researchers at Cincinnati Children’s infected pregnant mice with listeria and observed that subsets of immune cells subsequently attacked the placenta. These cells generated high levels of the chemoattractant protein CXCL9, which then triggered T-cells to target the fetus.

According to a 2012 study by researchers at New York University, in a healthy pregnancy, the parts of the immune system that would recognize the fetus as foreign are restricted from the placenta because CXCL9 is silenced from expression in the protective lining of the uterus, the decidua. But when infection occurs, CXCL9 and other chemoattractant proteins in the decidua activate, thereby breaking down that protective barrier for the fetus, which leads to birth abnormalities and fetal loss.

“One of the major misconceptions I would say is that when a microbe causes pregnancy complications, it’s directly related to the microbe invading the placenta and the fetus,” Way said, “but what we’ve shown is that many times when pregnancy complications are triggered by maternal infection, the injury of the fetus is not caused by the microbe— it’s caused by the maternal immune system being reprogrammed to reject the fetus.”

Way said multiple factors play a role in the development of birth abnormalities but that most experts agree infection is the driving force. Many times when women have symptoms of infection during pregnancy, doctors aren’t able to identify the microbe responsible. Study authors used the bacteria associated with listeria in their study because it’s easily executed in mouse models.

During their study, researchers at Cincinnati Children’s proved in two separate mice groups that by neutralizing CXCL9 activity and blocking its receptor on T cells, CXCR3, they protected the fetus from the mother’s immune system when a microbe was introduced to the body.

The first group of mice they studied was genetically modified to lack the CXCR3 chemokine receptor, so the harmful immune cells didn’t attack the fetuses during the listeria infection. In another group, researchers gave the pregnant, infected mice a protein or antibody with CXCR3-neutralizing properties, and saw that this therapeutic approach prevented stillbirth.

In a separate part of the study, researchers found that blocking a subset of maternal T cells would prevent stillbirth linked not to infection but to pregnancy complications like preeclampsia — a condition characterized by the mother’s high blood pressure and fluid retention— as well as spontaneous abortion. Way noted that, while this method wouldn’t be applicable to humans because eliminating these T cells would render mothers susceptible to other infections, the therapeutic approach holds potential for future treatment.