Sammanfattning

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.
Originalspråkengelska
Artikelnummer2630
TidskriftFrontiers in Immunology
Volym9
Antal sidor8
ISSN1664-3224
DOI
StatusPublicerad - 13 nov 2018
MoE-publikationstypA2 Granska artikel i en vetenskaplig tidskrift

Vetenskapsgrenar

  • 3123 Kvinno- och barnsjukdomar
  • 3111 Biomedicinska vetenskaper

Citera det här

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title = "The Immunogenetic Conundrum of Preeclampsia",
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.",
keywords = "preeclampsia, genetics, complement, major histocompatibility complex, FLT1, autoimmunity, pregnancy, HEMOLYTIC-UREMIC SYNDROME, COFACTOR PROTEIN CD46, SYSTEMIC-LUPUS-ERYTHEMATOSUS, COMPLEMENT ACTIVATION, ANGIOGENIC FACTORS, EARLY GESTATION, MATERNAL KIR, HLA-G, PREGNANCY, CELLS, 3123 Gynaecology and paediatrics, 3111 Biomedicine",
author = "Lokki, {A. Inkeri} and Heikkinen-Eloranta, {Jenni K.} and Hannele Laivuori",
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journal = "Frontiers in Immunology",
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The Immunogenetic Conundrum of Preeclampsia. / Lokki, A. Inkeri; Heikkinen-Eloranta, Jenni K.; Laivuori, Hannele.

I: Frontiers in Immunology, Vol. 9, 2630, 13.11.2018.

Forskningsoutput: TidskriftsbidragÖversiktsartikelVetenskapligPeer review

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AU - Heikkinen-Eloranta, Jenni K.

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N2 - 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.

AB - 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.

KW - preeclampsia

KW - genetics

KW - complement

KW - major histocompatibility complex

KW - FLT1

KW - autoimmunity

KW - pregnancy

KW - HEMOLYTIC-UREMIC SYNDROME

KW - COFACTOR PROTEIN CD46

KW - SYSTEMIC-LUPUS-ERYTHEMATOSUS

KW - COMPLEMENT ACTIVATION

KW - ANGIOGENIC FACTORS

KW - EARLY GESTATION

KW - MATERNAL KIR

KW - HLA-G

KW - PREGNANCY

KW - CELLS

KW - 3123 Gynaecology and paediatrics

KW - 3111 Biomedicine

U2 - 10.3389/fimmu.2018.02630

DO - 10.3389/fimmu.2018.02630

M3 - Review Article

VL - 9

JO - Frontiers in Immunology

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SN - 1664-3224

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