Question: Where do extraembryonic fetal stem cells come from?
About the article "Stem cell", section "Fetal".

Candidate passages:
The primitive stem cells located in the organs of fetuses are referred to as fetal stem cells.
There are two types of fetal stem cells:
 Fetal proper stem cells come from the tissue of the fetus proper, and are generally obtained after an abortion.
These stem cells are not immortal but have a high level of division and are multipotent.
 Extraembryonic fetal stem cells come from extraembryonic membranes, and are generally not distinguished from adult stem cells.
These stem cells are acquired after birth, they are not immortal but have a high level of cell division, and are pluripotent.
Recent studies have discovered that chorionic villi can be a rich source of fetal stem cells, multipotent mesenchymal stem cells A potential benefit of using fetal stem cells over those obtained from embryos is that they side-step ethical concerns among anti-abortion activists by obtaining pluripotent lines of undifferentiated cells without harm to a fetus or destruction of an embryo.
These stem cells would also, if used to treat the same individual they came from, sidestep the donor/recipient issue which has so far stymied all attempts to use donor-derived stem cells in therapies.
Artificial heart valves, working tracheas, as well as muscle, fat, bone, heart, neural and liver cells have all been engineered through use of fetal stem cells The first fetal stem cells bank in US is active in Boston, Massachusetts. 
"Potency" specifies the differentiation potential (the potential to differentiate into different cell types) of the stem cell.
Totipotent (a.k.a.
omnipotent) stem cells can differentiate into embryonic and extraembryonic cell types.
Such cells can construct a complete, viable organism.
These cells are produced from the fusion of an egg and sperm cell.
Cells produced by the first few divisions of the fertilized egg are also totipotent.
Pluripotent stem cells are the descendants of totipotent cells and can differentiate into nearly all cells, i.e.
cells derived from any of the three germ layers.
Multipotent stem cells can differentiate into a number of cell types, but only those of a closely related family of cells.
Oligopotent stem cells can differentiate into only a few cell types, such as lymphoid or myeloid stem cells.
Unipotent cells can produce only one cell type, their own, but have the property of self-renewal, which distinguishes them from non-stem cells (e.g.
progenitor cells, muscle stem cells).  
Types of microchimerism.
In humans (and perhaps in all Placentals) the most common form is fetomaternal microchimerism (also known as fetal cell microchimerism or fetal chimerism) whereby cells from a fetus pass through the placenta and establish cell lineages within the mother.
Fetal cells have been documented to persist and multiply in the mother for several decades.
The exact phenotype of these cells is unknown, although several different cell types have been identified, such as various immune lineages, mesenchymal stem cells, and placental-derived cells.
The potential health consequences of these cells are currently unknown.
One hypothesis is that these fetal cells might trigger a graft-versus-host reaction leading to autoimmune disease.
This offers a potential explanation for why many autoimmune diseases are more prevalent in middle-aged women.
The other main theory is that fetal cells home to injured or diseased maternal tissue where they act as stem cells and participate in repair.
It is also possible that the fetal cells are merely innocent bystanders and have no effect on maternal health.
After giving birth, about 50-75% of women carry fetal immune cell lines.
Maternal immune cells are also found in the offspring yielding in maternal→fetal microchimerism, though this phenomenon is about half as frequent as the former .
Microchimerism had also been shown to exist after blood transfusions to a severely immunocompromised population of patients who suffered trauma. 
Placental mechanisms.
The placenta functions as an immunological barrier between the mother and the fetus, creating an immunologically privileged site.
For this purpose, it uses several mechanisms: It secretes Neurokinin B containing phosphocholine molecules.
This is the same mechanism used by parasitic nematodes to avoid detection by the immune system of their host.
Also, there is presence of small lymphocytic suppressor cells in the fetus that inhibit maternal cytotoxic T cells by inhibiting the response to interleukin 2.
The placental trophoblast cells do not express the classical MHC class I isotypes HLA-A and HLA-B, unlike most other cells in the body, and this absence is assumed to prevent destruction by maternal cytotoxic T cells, which otherwise would recognize the fetal HLA-A and HLA-B molecules as foreign.
On the other hand, they do express the atypical MHC class I isotypes HLA-E and HLA-G, which is assumed to prevent destruction by maternal NK cells, which otherwise destroy cells that do not express any MHC class I.
However, trophoblast cells do express the rather typical HLA-C.
It forms a syncytium without any extracellular spaces between cells in order to limit the exchange of migratory immune cells between the developing embryo and the body of the mother (something an epithelium will not do sufficiently, as certain blood cells are specialized to be able to insert themselves between adjacent epithelial cells).
The fusion of the cells is apparently caused by viral fusion proteins from endosymbiotic endogenous retrovirus (ERV).
An immunoevasive action was the initial normal behavior of the viral protein, in order to avail for the virus to spread to other cells by simply merging them with the infected one.
It is believed that the ancestors of modern viviparous mammals evolved after an infection by this virus, enabling the fetus to better resist the immune system of the mother.
Still, the placenta does allow maternal IgG antibodies to pass to the fetus to protect it against infections.
However, these antibodies do not target fetal cells, unless any fetal material has escaped across the placenta where it can come in contact with maternal B cells and make those B cells start to produce antibodies against fetal targets.
The mother does produce antibodies against foreign ABO blood types, where the fetal blood cells are possible targets, but these preformed antibodies are usually of the IgM type, and therefore usually do not cross the placenta.
Still, rarely, ABO incompatibility can give rise to IgG antibodies that cross the placenta, and are caused by sentitization of mothers (usually of blood type 0) to antigens in foods or bacteria.