Relationship between Maternal Immunological Response during Pregnancy and Onset of Preeclampsia

Figure 1

Maternofetal immune response in preeclampsia. A series of events occurs in the maternal-fetal interface in preeclampsia that result in an altered expression of different factors (PIGF, sENG, sFLT1, GM-CSF, and TLR-4) as compared to normal pregnancies. Similarly, the ratio among various populations of immune cells (Th17/Treg, Th1/Th2) differs from normality in preeclamptic patients. Regarding the complement system, preeclampsia enhances MBL and C5a synthesis. These changes are evidenced in peripheral blood in which the proinflammatory systemic environment is also seen with high IL-6 a, TNF-alpha, IL-8, IP-10, MCP-1, ICAM-1, and VCAM-1 levels. Treg: CD4+CD25+Foxp3+ T regulatory cells; TLR: toll-like receptor; HLA: the human leukocyte antigen; uNk cell: uterine natural killer cell; KIR: killer immunoglobulin-like receptor; sFLT1: soluble fms-like tyrosine kinase-1 factor; sENG: soluble endoglin; PIGF: placenta growth factor; GM-CSF: granulocyte-macrophage colony-stimulating factor; MBL: mannose-binding lectin; Th cell: T helper cell; IL: interleukin; IFNg: interferon gamma; TNF-alpha: tumor necrosis factor alpha; IP-10: interferon-inducible-protein-10; MCP-1: monocyte chemotactic protein-1; ICAM-1: intercellular adhesion molecule 1; VCAM-1: vascular cell adhesion protein 1; Th17: a subpopulation of TCD4+ effector cells, Thelper 17 cells.