LOL! This is where PE gets messy.
The placenta is formed from the blastocyst, specifically from the outer cells of the blastocyst, which are a specific kind of cell called a trophoblast. Scientists had trouble establishing trophoblastic cell lines for study in the lab, because those cells have evolved to thrive in a very particular environment, inside the mother and particularly inside her decidua, the lining of the uterus that's shed each month in your period. (Total nerds like me will say "aha!" when I say that one of our "pseudotrophoblastic" cell lines turned out to just be HeLa.)
Once the blastocyst has landed - that's a quote from the caption of this Lennart Nilsson photo
- the trophoblastic cells embed into the uterus and establish the placenta. They're really just paternal cells, not fetal cells, because they've been epigenetically imprinted to shut down the expression of the maternal genes. And this is where the term "maternal-fetal conflict" comes from. They have Plans about how much blood flow the fetus will ultimately get. The mother's immune system has a different set of Plans, because she also wants the fetus to *fit out* once delivery rolls around.
The first order of business for the trophoblastic cells isn't to remodel the spiral arteries or start building the placenta, though it will do those shortly. The first thing is to coax the maternal immune system into ignoring the foreign proteins it's expressing. We do not entirely understand how this works, and scientific investigation into the question is obviously very difficult. But we do know that it communicates with the maternal decidual natural killer cells and talks them into *helping it* build the placenta.
There's some very interesting work coming out of Cambridge on this. The maternal KIR are polymorphic - that means that a bunch of different versions show up in humans. The paternal HLA is also polymorphic. KIR AA phenotype coupled to HLA-C is much more likely to lead to PE pregnancies, probably because the receptors simply cannot accept the molecule that serves the function of modulating some of the immune response, because the shape of the receptor cannot accomodate the shape of the antigen.
This means while it isn't *entirely* the dad's fault all the time, if he's making HLA-C and you're carrying KIR-AA, it can be partly his fault. ("Honey! It's your fault!")
(Funky philosophical concepts here include altruism, speciation, and functions. Your mileage may vary!)