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Biochemistry - Immunology - Obstetrics - Physiology

Placental Expression of CD100, CD72 and CD45 Is Dysregulated in Human Miscarriage
Published: Friday, May 11, 2012
Author: Teresa Lorenzi et al.

by Teresa Lorenzi, Angelo Turi, Maria Lorenzi, Francesca Paolinelli, Francesca Mancioli, Lucia La Sala, Manrico Morroni, Pasquapina Ciarmela, Angelo Mantovani, Andrea Luigi Tranquilli, Mario Castellucci, Daniela Marzioni

Context and Objective

The 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.


Placenta 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.


CD100, 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.


Fetal 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.