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| Research article summary (published 4 May 2006): |
Inflammation and miscarriage.
Full 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.
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Author information
Author/s: Christiansen, Ole B (OB); Nielsen, Henriette S (HS); Kolte, Astrid M (AM);
Affiliation: Fertility Clinic 4071, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. obc(-atsign-)pregnancyloss.dk
Journal and publication information
Publication Type: Journal Article; Review
Journal: Seminars in fetal & neonatal medicine (Semin Fetal Neonatal Med), published in Netherlands. (Language: eng)
Reference: 2006-Oct; vol 11 (issue 5) : pp 302-8
Dates: Created 2006/07/18; Completed 2007/02/27;
PMID: 16682265, status: MEDLINE (last retrieval date: 12/26/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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