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Immunology of preeclampsia
Linköpings universitet, Institutionen för molekylär och klinisk medicin, Obstetrik och gynekologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
Linköpings universitet, Institutionen för molekylär och klinisk medicin, Obstetrik och gynekologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Kvinnokliniken i Linköping.
Linköpings universitet, Institutionen för molekylär och klinisk medicin, Klinisk immunologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk immunologi och transfusionsmedicin.
Linköpings universitet, Institutionen för molekylär och klinisk medicin, Klinisk immunologi. Linköpings universitet, Hälsouniversitetet.ORCID-id: 0000-0002-3993-9985
Vise andre og tillknytning
2005 (engelsk)Inngår i: Immunology of Pregnancy / [ed] Markert U.R. (Jena), Basel, Switzerland: S. Karger, 2005, Vol. 89, s. 49-61Kapittel i bok, del av antologi (Fagfellevurdert)
Abstract [en]

Preeclampsia is a placenta-dependent disorder with both local and systemic anomalies with neonatal and maternal morbidity. It is manifested late in pregnancy, but the onset is during early stages of gestation. The current hypothesis regarding the aetiology of preeclampsia is focused on maladaptation of immune responses and defective trophoblast invasion. Thus, an excessive maternal inflammatory response, perhaps directed against foreign fetal antigens, results in a chain of events including shallow trophoblast invasion, defective spiral artery remodelling, placental infarction and release of pro-inflammatory cytokines and placental fragments in the systemic circulation. During normal pregnancy, trophoblasts interact in the decidua with the unique uterine NK cells, modifying their cytokine repertoire, regulating adhesion molecules and matrix metalloproteinases. The inability of trophoblasts to accomplish these changes might be a critical factor for the onset of preeclampsia. Several cytokines, produced at the maternal-fetal interface, have an impact on trophoblast invasion. It is suggested that deficiency of interleukin-10 may contribute to enhanced inflammatory responses towards the trophoblasts elicited by e.g. tumour necrosis factor-α and interferon-γ. Consequently, trophoblasts subjected to a high rate of apoptosis are hampered in their invasive capacity resulting in defective transformation of spiral arteries, hypoxia, thrombosis and infarction of the placenta. The ensuing infarction of placenta leads to leakage of increasing amounts of placental fragments and cytokines in the maternal circulation and an exaggerated systemic endothelial activation as identified in preeclampsia. So far, treatment of preeclampsia is focused on signs like hypertension, whereas attempts of modifying immune responses may be a possibility in the future.

sted, utgiver, år, opplag, sider
Basel, Switzerland: S. Karger, 2005. Vol. 89, s. 49-61
Serie
Chemical Immunology and Allergy, ISSN 1660-2242 ; Vol. 89
HSV kategori
Identifikatorer
URN: urn:nbn:se:liu:diva-29576DOI: 10.1159/000087912PubMedID: 16129952Lokal ID: 14952ISBN: 978-3-8055-7970-4 (tryckt)ISBN: 978-3-318-01248-4 (tryckt)OAI: oai:DiVA.org:liu-29576DiVA, id: diva2:250393
Tilgjengelig fra: 2009-10-09 Laget: 2009-10-09 Sist oppdatert: 2014-06-18bibliografisk kontrollert

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