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Keywords:

  • Pre-eclampsia;
  • Toll-like receptors signaling

Systemic inflammation and abnormal/poor placentation represent hallmarks of pre-eclampsia. Accumulating evidence suggests that infectious agents might increase the risk of pre-eclampsia; the innate immune defense mechanisms may interact with pro-inflammatory pathways, and contribute to the development of pre-eclampsia. The evidence for this has been supported by indirect epidemiologic and clinical studies, as well as by some direct support from experimental studies. Recent data directly implicate signaling by Toll-like receptors in the pathogenesis of pre-eclampsia, and establish a crucial link between pre-eclampsia and defense against both foreign pathogens and endogenously generated inflammatory ligands. Here, we review the rapid progress in this field, which has improved our understanding of the interplay between pathogen invasion, innate immune defense mechanisms, and pre-eclampsia.