Microvesicles (MVs) can derive from several cell types and their membranes contain
cell surface elements. Their role is increasingly recognized in cell-to-cell communication,
as they act as both paracrine and remote messengers, occurring in circulating form
as well as in plasma. Successful pregnancy requires a series of interactions between
the maternal immune system and the implanted fetus, such that the semi-allograft will
not be rejected. These interactions occur at the materno-placental interface and/or
at a systemic level. In the present study we identified for the first time the in
vivo plasma pattern of the MVs of third-trimester, healthy pregnant women, their cellular
origin, and their target cells using flow cytometry and confocal laser microscopy.
We searched for the cellular target molecules of thrombocyte-derived MVs with the
help of neutralizing antibodies. We examined the in vitro effects of MVs on STAT3
phosphorylation of primary lymphocytes and Jurkat cells. We found that both placental
trophoblast-derived and maternal thrombocyte-derived MVs bind to circulating peripheral
T lymphocytes, but not to B lymphocytes or NK cells. We were able to show that the
P-selectin (CD62P)-PSGL-1 (CD162) interaction is one mechanism binding platelet-derived
MVs to T cells. We were also able to demonstrate that MV-lymphocyte interactions induce
STAT3 phosphorylation in T cells. Our findings indicate that both thrombocyte- and
trophoblast-derived MVs may play an important role in the immunomodulation of pregnancy.
We suggest that the transfer of different signals via MVs represents a novel form
of communication between the placenta and the maternal immune system, and that MVs
contribute to the establishment of stable immune tolerance to the semi-allograft fetus.