Inflammation and miscarriage

Ole B Christiansen, Henriette S Nielsen, Astrid M Kolte

    105 Citationer (Scopus)

    Abstract

    Most relevant studies in animals and humans indicate that some degree of systemic or uterine inflammation is necessary both for normal implantation and pregnancy. However, if inflammation becomes too excessive it might cause pregnancy complications such as fetal resorption/miscarriage. The main regulator of the correct level of inflammation at the feto-maternal interface seems to be the uterine CD16(-) CD56(bright) natural killer (NK) cells. Trophoblast debris, apoptotic cells and progesterone probably stimulate/regulate the production of inflammatory cytokines from these cells. Miscarriage of karyotypically normal embryos may occur when the level of inflammation at the feto-maternal interface falls outside the optimal range. This may be caused by an insufficient influx of CD56(bright) NK cells into the decidua, too little soluble histocompatibility leukocyte antigen (HLA)-G secretion from the trophoblast, hypersecretion of inflammatory cytokines due to the presence of high-production polymorphisms, presence of maternal HLA-DR alleles associated with high tumor necrosis factor (TNF)-alpha production, or maternal mannose-binding lectin deficiency.

    OriginalsprogEngelsk
    TidsskriftSeminars in Fetal & Neonatal Medicine
    Vol/bind11
    Udgave nummer5
    Sider (fra-til)302-8
    Antal sider7
    ISSN1744-165X
    DOI
    StatusUdgivet - okt. 2006

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