Abstract
The complement system plays a double role in pregnancy exerting both protective and damaging effects at placental level. Complement activation at fetal-maternal interface participates in protection against infectious agents and helps remove apoptotic and necrotic cells. Locally synthesized C1q contributes to the physiologic vascular remodeling of spiral arteries characterized by loss of smooth muscle cells and transformation into large dilated vessels. Complement activation triggered by the inflammatory process induced by embryo implantation can damage trophoblast and other decidual cells that may lead to pregnancy complications if the cells are not protected by the complement regulators CD55, CD46, and CD59 expressed on cell surface. However, uncontrolled complement activation induces placental alterations resulting in adverse pregnancy outcomes. This may occur in pathological conditions characterized by placental localization of complement fixing antibodies directed against beta2-glycoprotein 1, as in patients with anti-phospholipid syndrome, or circulating immune complexes deposited in placenta, as in patients with systemic lupus erythematosus. In other diseases, such as preeclampsia, the mechanism of complement activation responsible for complement deposits in placenta is unclear. Conflicting results have been reported on the relevance of complement assays as diagnostic and prognostic tools to assess complement involvement in pregnant patients with these disorders.
Highlights
Motherhood has become a feasible option in recent years even for women with rheumatic diseases, thanks to the marked improvement in the diagnostic modalities and therapeutic approaches developed in the field of rheumatology
Despite the progress made in recent years, pregnancies in these conditions are still burdened by a high rate of obstetric complications, mainly in terms of preeclampsia, preterm delivery, and intrauterine growth restriction (IUGR) [4] and a tight control is recommended for a positive pregnancy outcome [4, 5]
C5b-9 was detected in all placentae and was localized on the surface of syncytiotrophoblasts, intervillous fibrin and decidual vessels supporting its contribution to tissue damage. These findings suggest that complement activation is involved in placental pathology acting both on villous trophoblast and on endothelial cells of decidual vessels (Figure 3)
Summary
Motherhood has become a feasible option in recent years even for women with rheumatic diseases, thanks to the marked improvement in the diagnostic modalities and therapeutic approaches developed in the field of rheumatology. Animal models have shown that C1q-deficient pregnant mice manifest the key features of human disease such as hypertension, albuminuria, endothelial dysfunction, decreased placental vascular endothelial growth factor, and elevated levels of sFlt-1 providing convincing evidence that C1q protects against pre-eclampsia [31] Consistent with this in vivo observation, Agostinis, and colleagues [17] published data indicating that the serum levels of C1q was markedly decreased in both early and late onset forms of pre-eclampsia. Antibodies against β2GPI co-localize with their target antigen on trophoblasts and decidual endothelial cells in immunized animals that had received fluorescein-labeled β2GPI [46] and interfere with pregnancy progression by impairing the function of the developing placenta The antibodies exert their effect on the maternal side, promoting a negative imbalance of angiogenic factors that inhibits endometrial angiogenesis.
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