So, to outwit the mother's lymphocytes, the father's trophoblasts create a diversion. Trophoblasts make a protein (PP13), which exits the blood vessels and travels into the lining of the uterus.
The lymphocytes rush to deal with that inflammation, ignoring the trophoblasts.
"All of the mother's soldiers are being diverted and focusing on the PP13 instead of going after the trophoblasts," Kliman said. "It's very sneaky."
The findings are published in the Oct. 11 online issue of Reproductive Sciences.
In the study, researchers used placental tissue from women in the United States and Israel.
Prior research had found that when levels of the PP13 protein are low early in pregnancy, women were more likely to develop preeclampsia several months later, but why PP13 contributed to that wasn't understood.
Kliman said the molecular battle is driven by the father-directed trophoblasts, which are trying to create conditions for a big, healthy baby, while mother needs to tamp down on growth so that the fetus is small enough to get through the birth canal.
"The mother does not want to die. The father wants a big baby. So they compromise," he said. "If the invasive trophoblasts are killed, the blood vessels wouldn't open up, and the baby would die. If the father wins the battle and the trophoblasts are able to go into the uterus, the baby would grow too big and the woman would die."
Dr. Jill Rabin, chief of ambulatory care in the obstetrics and gynecology department and head of urogynecology at Long Island Jewish Medical Center in New Hyde Park, N.Y., said the research adds "teeth" to the theory of the role of trophoblasts in preeclampsia.
"It makes a lot of sense that the mother's immune system had to be tricked somehow, otherwise how
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