Abstract
Context and ObjectiveThe etiology of miscarriage is often multifactorial. One major cause, immunological rejection of the fetus, has not been clearly elucidated. Our aim was to establish whether the semaphorin CD100, its natural receptor CD72, and the glycoprotein CD45, implicated in immune mechanisms, are involved in pregnancy loss by examining their placental expression with real-time PCR, immunohistochemistry and western blotting techniques.PatientsPlacenta tissue from 72 Caucasian women undergoing surgical uterine evacuation due to early spontaneous pregnancy loss between the 8th and 12th week of gestation was divided into four groups based on miscarriage number. Gestational age-matched placentas from 18 healthy women without a history of miscarriage undergoing voluntary pregnancy termination were the control group. Placenta from 6 Caesarean deliveries performed at 38–40 weeks of gestation was also studied.ResultsCD100, CD72 and CD45 were expressed in placenta and exhibited different mRNA and protein levels in normal pregnancy and miscarriage. In particular, protein levels were highly dysregulated around 10 weeks of gestation in first and second miscarriage placentas. The CD100 soluble form was produced and immediately shed from placental tissue in all samples.ConclusionsFetal CD100, CD72 and CD45 seem to play a role in miscarriage. The present data support the involvement of the fetal immune system in pregnancy maintenance as well as failure.
Highlights
Miscarriage is a frequent event in human pregnancy
CD100, CD72 and CD45 were expressed in placenta and exhibited different mRNA and protein levels in normal pregnancy and miscarriage
Fetal CD100, CD72 and CD45 seem to play a role in miscarriage
Summary
Miscarriage (fetal death before 24 weeks of gestation, w.g.) is a frequent event in human pregnancy. In a normal pregnancy the maternal immune system is not suppressed; on the contrary, it is capable of efficiently recognizing and reacting against foreign antigens of the ‘‘fetal transplant’’ [10]. The goal of the maternal response is to avoid extravillous trophoblast cell over-invasion [11], balancing womb integrity and fetal nutrition [12]. Such balance is realized by the development by maternal leukocytes of tolerance for the antigens expressed in the semi-allogeneic/allogeneic fetal cells. Shao L. et al [14] noted that human placental trophoblasts activate a particular type of T cells that modulate T cell-dependent B cell responses, resulting in efficient suppression of Ig secretion. The fetal mechanisms that circumvent the maternal immune response in the pregnant uterus are still unclear
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