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WFRF:(Matthiesen Leif)
 

Sökning: WFRF:(Matthiesen Leif) > (2005-2009) > Immunology of preec...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003943naa a2200349 4500
001oai:DiVA.org:liu-29576
003SwePub
008091009s2005 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-295762 URI
024a https://doi.org/10.1159/0000879122 DOI
040 a (SwePub)liu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a kap2 swepub-publicationtype
100a Matthiesen, Leif,d 1954-u Östergötlands Läns Landsting,Linköpings universitet,Obstetrik och gynekologi,Hälsouniversitetet,Kvinnokliniken i Linköping4 aut0 (Swepub:liu)leima96
2451 0a Immunology of preeclampsia
264 1a Basel, Switzerland :b S. Karger,c 2005
338 a print2 rdacarrier
520 a 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.
653 a MEDICINE
653 a MEDICIN
700a Berg, Göran,d 1946-u Östergötlands Läns Landsting,Linköpings universitet,Obstetrik och gynekologi,Hälsouniversitetet,Kvinnokliniken i Linköping4 aut0 (Swepub:liu)gorbe09
700a Ernerudh, Jan,d 1952-u Östergötlands Läns Landsting,Linköpings universitet,Klinisk immunologi,Hälsouniversitetet,Klinisk immunologi och transfusionsmedicin4 aut0 (Swepub:liu)janer15
700a Ekerfelt, Christina,d 1957-u Linköpings universitet,Klinisk immunologi,Hälsouniversitetet4 aut0 (Swepub:liu)chrek55
700a Jonsson, Yvonne,d 1974-u Linköpings universitet,Klinisk immunologi,Hälsouniversitetet4 aut0 (Swepub:liu)yvojo35
700a Sharma, Surendrau Department of Pediatrics and Pathology, Women and Infants Hospital of Rhode Island, Brown University, Providence, R.I., USA4 aut
710a Linköpings universitetb Obstetrik och gynekologi4 org
773t Immunology of pregnancyd Basel, Switzerland : S. Kargerg , s. 49-61q <49-61z 9783805579704z 9783318012484
856u https://libris.kb.se/bib/9991557y Find book at a swedish library/Hitta boken i ett svenskt bibliotek
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-29576
8564 8u https://doi.org/10.1159/000087912

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