Immunology of preeclampsia

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Matthiesen, Leif,1954-Östergötlands Läns Landsting,Linköpings universitet,Obstetrik och gynekologi,Hälsouniversitetet,Kvinnokliniken i Linköping (author)

Immunology of preeclampsia

Article/chapterEnglish2005

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Basel, Switzerland :S. Karger,2005
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LIBRIS-ID:oai:DiVA.org:liu-29576
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-29576URI
https://doi.org/10.1159/000087912DOI

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Language:English
Summary in:English

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Subject category:ref swepub-contenttype
Subject category:kap swepub-publicationtype

Notes

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.

Subject headings and genre

MEDICINE
MEDICIN

Added entries (persons, corporate bodies, meetings, titles ...)

Berg, Göran,1946-Östergötlands Läns Landsting,Linköpings universitet,Obstetrik och gynekologi,Hälsouniversitetet,Kvinnokliniken i Linköping(Swepub:liu)gorbe09 (author)
Ernerudh, Jan,1952-Östergötlands Läns Landsting,Linköpings universitet,Klinisk immunologi,Hälsouniversitetet,Klinisk immunologi och transfusionsmedicin(Swepub:liu)janer15 (author)
Ekerfelt, Christina,1957-Linköpings universitet,Klinisk immunologi,Hälsouniversitetet(Swepub:liu)chrek55 (author)
Jonsson, Yvonne,1974-Linköpings universitet,Klinisk immunologi,Hälsouniversitetet(Swepub:liu)yvojo35 (author)
Sharma, SurendraDepartment of Pediatrics and Pathology, Women and Infants Hospital of Rhode Island, Brown University, Providence, R.I., USA (author)
Linköpings universitetObstetrik och gynekologi (creator_code:org_t)

Related titles

In:Immunology of pregnancyBasel, Switzerland : S. Karger, s. 49-6197838055797049783318012484

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https://libris.kb.se/bib/9991557Find book at a swedish library/Hitta boken i ett svenskt bibliotek
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-29576
https://doi.org/10.1159/000087912

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