TY - JOUR
T1 - Inflammation and miscarriage
AU - Christiansen, Ole B
AU - Nielsen, Henriette S
AU - Kolte, Astrid M
PY - 2006/10
Y1 - 2006/10
N2 - 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.
AB - 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.
KW - Abortion, Habitual/etiology
KW - Abortion, Spontaneous/etiology
KW - Animals
KW - Anti-Inflammatory Agents/therapeutic use
KW - CD56 Antigen/physiology
KW - Cytokines/physiology
KW - Female
KW - HLA Antigens/metabolism
KW - HLA-G Antigens
KW - Histocompatibility Antigens Class I/metabolism
KW - Humans
KW - Inflammation/complications
KW - Killer Cells, Natural/physiology
KW - Mannose-Binding Lectin/physiology
KW - Pregnancy
KW - Pregnancy Complications/etiology
U2 - 10.1016/j.siny.2006.03.001
DO - 10.1016/j.siny.2006.03.001
M3 - Review
C2 - 16682265
SN - 1744-165X
VL - 11
SP - 302
EP - 308
JO - Seminars in Fetal & Neonatal Medicine
JF - Seminars in Fetal & Neonatal Medicine
IS - 5
ER -