Which is the most prominent feature of the disease. Some candidates for these unknown ‘preeclampsia factors’ include pro-inflammatory cytokines, microparticles and anti-angiogenic factors. An imbalance between pro-angiogenic factors such as vascular endothelial growth factor and placental growth factor, and anti-angiogenic factors such as soluble fms-like tyrosine kinase 1 and soluble endoglin, has been observed before the onset of PE and after the clinical diagnosis. Endoglin, or CD105, is a homodimeric transmembrane glycoprotein localized on cell surfaces that functions as a coreceptor for transforming growth factor -b1 and TGF-b3 isoforms. Soluble endoglin might play an antiangiogenic effect in PE through binding to circulating TGF-b1, thus preventing its interaction with cell membrane, and consequently the pro-angiogenic and vasodilators effects of TGF-b1 in the normal endothelium. Previous studies demonstrated the involvement of TGF-b1 in the pathophysiology of PE but the results are conflicting. Some studies have found higher levels of TGF-b1 in PE, while in others there was no difference between PE and normotensive pregnancies. It is well established that an excessive maternal systemic inflammatory response to pregnancy is also involved in the pathogenesis of PE. Our research group has previously reported higher levels of pro-inflammatory cytokines, and decreased levels of the anti-inflammatory cytokine IL-10 in PE. Other studies have also reported that maternal circulating concentration of TNF soluble receptors sTNF-R1 and sTNF-R2 are significantly increased in preeclamptic and normotensive pregnant women under risk to develop this disease. The aim of this study was to evaluate the sEng, TGF-b1, sTNFR1 and sTNFR-2 levels in different forms of PE and to compare these variables to normotensive pregnant and healthy nonpregnant women, aiming to better understand the role of inflammation and endothelial dysfunction in PE pathogenesis. Our findings suggest that pregnancy is a condition associated with higher levels of anti-angiogenic and pro-inflammatory factors than the non-pregnant state and that PE is associated with an imbalance of these factors in the maternal circulation. In this study we compared the sEng, TGF-b1, sTNF-R1 and sTNFR-2 levels in women with different forms of PE, normotensive pregnant and healthy non-pregnant women. The past decades of research have brought a greater understanding of potential angiogenic imbalance that is likely involved in the PE pathophysiology. Eng is a pro-angiogenic agent that prevents apoptosis in hypoxic endothelial cells and is an essential component of the endothelial nitric oxide synthase activation complex, regulating nitric oxide-dependent regulation of vascular tone. In contrast, soluble Eng is an anti-angiogenic protein thought to impair TGF-b1 binding to its receptors and downstream signaling including effects on activation of eNOS and vasodilatation.