Abstract

Pregnancy is an immunological challenge to the mother. The fetal tissues including the placenta must be protected from activation of the maternal immune system. On the other hand, the placental tissue sheds into the maternal circulation and must be adequately identified and phagocytized by the maternal immune system. During a healthy pregnancy, numerous immunosuppressive processes take place that allow the allograft fetus to thrive under exposure to humoral and cellular components of the maternal immune system. Breakdown of immune tolerance may result in sterile inflammation and cause adverse pregnancy outcomes such as preeclampsia, a vascular disease of the pregnancy with unpredictable course and symptoms from several organs. Immunological incompatibility between mother and fetus is strongly indicated in preeclampsia. Recently, genetic factors linking immunological pathways to predisposition to preeclampsia have been identified. In this mini-review genetic variation in immunological factors are discussed in the context of preeclampsia. Specifically, we explore immunogenetic and immunomodulary mechanisms contributing to loss of tolerance, inflammation, and autoimmunity in preeclampsia.

Highlights

  • The Immunogenetic Conundrum of PreeclampsiaPregnancy is an immunological challenge to the mother

  • Preeclampsia is a heterogeneous vascular disease of the human pregnancy that presents in a previously normotensive woman during the second half of the pregnancy with hypertension and proteinuria, or preeclampsia-associated signs in the absence of proteinuria [1, 2]

  • Our group has published protective maternal low-frequency variants in the same gene [20]. In this mini-review we explore the immunogenetic role of Fms-like tyrosine kinase 1 (FLT1) in preeclampsia and selected genetic studies implicating loss of immune tolerance in early pregnancy or late pregnancy inflammation in preeclampsia

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Summary

The Immunogenetic Conundrum of Preeclampsia

Pregnancy is an immunological challenge to the mother. The placental tissue sheds into the maternal circulation and must be adequately identified and phagocytized by the maternal immune system. Numerous immunosuppressive processes take place that allow the allograft fetus to thrive under exposure to humoral and cellular components of the maternal immune system. Breakdown of immune tolerance may result in sterile inflammation and cause adverse pregnancy outcomes such as preeclampsia, a vascular disease of the pregnancy with unpredictable course and symptoms from several organs. Immunological incompatibility between mother and fetus is strongly indicated in preeclampsia. Genetic factors linking immunological pathways to predisposition to preeclampsia have been identified. In this mini-review genetic variation in immunological factors are discussed in the context of preeclampsia.

INTRODUCTION
IMMUNOGENETIC PREDISPOSITION FOR COMPROMISED TOLERANCE
Findings
CONCLUSION
Full Text
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