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Published on: May 21, 2015
Decoding the immunological triad of TLRs, B1 cells, and feto-maternal microchimerism in pre-eclampsia pathogenesis: a
Maithreyi Chandan Nair1, Kesar Chandel1, Shreevarsha S1
1School of Bio-sciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
Pre-eclampsia (PE) is a pregnancy-specific hypertensive disorder with fatal consequences for maternal and foetal health, including placental abruption, foetal growth restriction, and foetal death. Its global prevalence is estimated at 2-8%. While many aspects of PE pathogenesis are well-characterised, those pertaining to its immunology are less well understood. This review examines three interconnected aspects of the maternal immune microenvironment-toll-like receptors (TLRs), B1 cells, and feto-maternal microchimerism-and their role in PE pathogenesis. While each has been studied independently, no prior review has examined these three components as an interacting system. TLRs function as endogenous danger-molecule sensors, with pathological activation of TLR7 and TLR9 facilitating overzealous pro-inflammatory signalling, endothelial injury, and defective spiral-artery remodelling. B1 cells differentiate into a pathogenic phenotype during pathological pregnancies, secreting agonistic autoantibodies against the angiotensin II type 1 receptor (AT1-AA), associated with vasoconstriction and hypertension. Feto-maternal microchimerism generally serves to induce maternal immune tolerance towards foetal antigens. In PE pregnancies, increased trafficking of foetal cells has been shown to release cell-free foetal DNA into the maternal circulation, resulting in excessive activation of TLR-mediated sterile inflammation. This review explores the evidence for how these three factors may interact to create a positive feedback loop.
Pre-eclampsia (PE) is a pregnancy-specific hypertensive disorder with fatal consequences for maternal and foetal health, including placental abruption, foetal growth restriction, and foetal death. Its global prevalence is estimated at 2-8%. While many aspects of PE pathogenesis are well-characterised, those pertaining to its immunology are less well understood. This review examines three interconnected aspects of the maternal immune microenvironment-toll-like receptors (TLRs), B1 cells, and feto-maternal microchimerism-and their role in PE pathogenesis. While each has been studied independently, no prior review has examined these three components as an interacting system. TLRs function as endogenous danger-molecule sensors, with pathological activation of TLR7 and TLR9 facilitating overzealous pro-inflammatory signalling, endothelial injury, and defective spiral-artery remodelling. B1 cells differentiate into a pathogenic phenotype during pathological pregnancies, secreting agonistic autoantibodies against the angiotensin II type 1 receptor (AT1-AA), associated with vasoconstriction and hypertension. Feto-maternal microchimerism generally serves to induce maternal immune tolerance towards foetal antigens. In PE pregnancies, increased trafficking of foetal cells has been shown to release cell-free foetal DNA into the maternal circulation, resulting in excessive activation of TLR-mediated sterile inflammation. This review explores the evidence for how these three factors may interact to create a positive feedback loop.
