American journal of reproductive immunology (New York, N.Y. : 1989) · 2008
Distribution and maturity of dendritic cells in diseases of insufficient placentation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Scholz Christoph, Toth Bettina, Santoso Laura, Kuhn Christina, Franz Maximilian, Mayr Doris, Jeschke Udo, Friese Klaus, Schiessl Barbara
Аннотация
PROBLEM: The immunological equilibrium at the feto-maternal interphase contributes towards late gestational diseases like growth restriction (IUGR) pre-eclampsia (PE) and hemolysis, elevated liver enzymes, low platelets (HELLP)-syndrome. The state of activation of decidual dendritic cells (DC) has emerged as one of the central players influencing this immunological equilibrium.
METHOD OF STUDY: Paraffin-embedded tissue sections from 27 pregnancies were immunostained for DC markers DEC-205, DC-SIGN, DC-LAMP and costained for DC-SIGN/CD56 and DC-SIGN/ vascular endothelial growth factor receptor (VEGFR) -1 and -2. We investigated placental tissue of IUGR fetuses and of patients who developed PE or HELLP-syndrome as well as placental tissue derived from normal pregnancies.
RESULTS: We found that expression of DEC-205 and DC-SIGN was significantly upregulated in HELLP placentas, whereas expression of DC-LAMP was abrogated almost entirely. Costaining showed an interaction between DC-SIGN(+) DC and natural killer cells as well as costaining of VEGFR-1 and -2 and DC-SIGN. Pre-eclamptic and IUGR placentas showed no significant change in any of the investigated markers compared to normal controls.
CONCLUSION: Our data suggest a participation of DC-mediated immunological mechanisms in HELLP syndrome.
METHOD OF STUDY: Paraffin-embedded tissue sections from 27 pregnancies were immunostained for DC markers DEC-205, DC-SIGN, DC-LAMP and costained for DC-SIGN/CD56 and DC-SIGN/ vascular endothelial growth factor receptor (VEGFR) -1 and -2. We investigated placental tissue of IUGR fetuses and of patients who developed PE or HELLP-syndrome as well as placental tissue derived from normal pregnancies.
RESULTS: We found that expression of DEC-205 and DC-SIGN was significantly upregulated in HELLP placentas, whereas expression of DC-LAMP was abrogated almost entirely. Costaining showed an interaction between DC-SIGN(+) DC and natural killer cells as well as costaining of VEGFR-1 and -2 and DC-SIGN. Pre-eclamptic and IUGR placentas showed no significant change in any of the investigated markers compared to normal controls.
CONCLUSION: Our data suggest a participation of DC-mediated immunological mechanisms in HELLP syndrome.
Предметные рубрики MeSH
Antigens, CDCell Adhesion MoleculesDeciduaDendritic CellsFemaleFetal Growth RetardationHELLP SyndromeHumansKiller Cells, NaturalLectins, C-TypeLysosomal Membrane ProteinsMinor Histocompatibility AntigensPlacentationPre-EclampsiaPregnancyReceptors, Cell SurfaceReceptors, Vascular Endothelial Growth FactorDC-Specific ICAM-3 Grabbing Nonintegrin