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Alterations in the Expression of Homing-Associated Molecules at the Maternal/Fetal Interface During the Course of Pregnancy
Ist Teil von
Biology of reproduction, 2002-02, Vol.66 (2), p.333-345
Ort / Verlag
Madison, WI: Society for the Study of Reproduction
Erscheinungsjahr
2002
Quelle
MEDLINE
Beschreibungen/Notizen
One of the most fascinating immunologic questions is how the genetically distinct fetus is able to survive and develop within
the mother without provoking an immune rejection response. The pregnant uterus undergoes rapid morphological and functional
changes, and these changes may influence the nature of local immune responses at the maternal/fetal interface at different
stages of gestation. We hypothesized that specialized mechanisms exist to control access of maternal leukocyte subsets to
the decidua and that these mechanisms are modulated during the course of pregnancy. At the critical period of initial placenta
development, the maternal/fetal interface displays an unparalleled compartmentalization of microenvironmental domains associated
with highly differentiated vessels expressing vascular addressins in nonoverlapping patterns and with recruitment of specialized
leukocyte subsets (monocytes, granulated metrial gland cells, and granulocytes) thought to support, modulate, and regulate
trophoblast invasion. One of the most striking observations at this time of gestation is the almost complete exclusion of
lymphocytes from the maternal/fetal interface. The second half of pregnancy is characterized by a partial loss of microenvironmental
specialization and different switches in vascular specificity within the decidua basalis, paralleling dramatic changes in
the populations of recruited leukocytes (e.g., a striking influx of lymphocytes, especially T cells). In the term pregnant
uterus, the expression of all vascular addressins decreased dramatically; only weakly staining maternal vascular segments
remained. These segments may define sites of extremely low residual traffic in the term decidua, which contains remarkably
few maternal leukocytes overall. Our results suggest that the maternal/fetal interface represents a situation in which leukocyte
trafficking is exquisitely regulated to allow entry of specialized leukocyte subsets that may play a fundamental role in immune
regulation during pregnancy.