Complement Factor B Activation in Patients with Preeclampsia

Preeclampsia is a leading cause of maternal and fetal morbidity and mortality. Its cause remains poorly understood and is likely multifactorial (reviewed in depth elsewhere) (Ahn et al., 2011, Robillard et al., 2014). Briefly, deficient trophoblastic invasion of the uterine spiral arteries results in inadequate placentation, leading to placental hypoxia and ischemia (Roberts and Bell, 2013, Saito and Nakashima, 2014). These events, in turn, alter the maternal immune system, including activation of immune cells (e.g., NK cells, dendritic cells, neutrophils, B and T lymphocytes), releasing lipid peroxidation by-products, anti-angiogenic, autoimmune, and proinflammatory factors (e.g., sFlt-1, s-endoglin, AT1-AA, aPL, TNF-α, IL-1β, IL-6, IL-10, IL-17, IL-18, and microRNA) (Ahn et al., 2011, Robillard et al., 2014).

Source: Journal of Reproductive Immunology - January 2, 2015 Category: Allergy & Immunology Authors: Ivan Velickovic, Mudar Dalloul, Karen A. Wong, Olufunke Bakare, Franz Schweis, Maya Garala, Amit Alam, Giorgio Medranda, Jovana Lekovic, Waqas Shuaib, Andreas Tedjasukmana, Perry Little, Daniel Hanono, Ruvini Wijetilaka, Jeremy Weedon, Jun Lin, Roulhac dâ Source Type: research