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The theory that links microchimerism to scleroderma is roughly as follows:
- During any pregnancy, cells of both the pregnant mother and the unborn child pass naturally back and forth between them through blood circulation. This causes microchimerism, with low levels of both the mother's and the baby's cells existing in each other's body.
- In most mothers, their immune systems eliminate these foreign fetal cells within a few months of the birth of the child.
- Some studies on women with scleroderma, however, have detected small but significant numbers of fetal cells decades after pregnancies with male babies. Furthermore, the DNA in such fetal cells often closely matches the mother's own DNA.
- This suggests, then, that the mother's immune system may not have recognized the fetal cells as being foreign and so did not eliminate them after birth. In addition, the similarity between the mother's and the fetal cells confused the immune system, so that the mother's own antibodies learned to attack not only the fetal cells but also her own as well.
On-going research is detecting a greater prevalence of fetal cells in women with scleroderma than in the general population. In 2002, for example, researchers detected microchimerism in the saliva gland cells of 45% of women with systemic sclerosis who had a history of pregnancy with male babies.
The following has been suggested to explain how microchimerism may trigger scleroderma in men or in women who had never been pregnant:
- The mother's cells pass into and persist in the bloodstream of the fetus. Her offspring then becomes at risk for scleroderma later on.
- Cells pass within the womb from one twin to another.
- Cells become transferred during blood transfusions or transplantation procedures.
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In any case, however, if microchimerism plays a role, it most likely does so only in a subset of patients.
Triggering the Immune Response
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