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ORIGINAL ARTICLE: Distribution and Maturity of Dendritic Cells in Diseases of Insufficient Placentation

Authors


  • This work is part of the doctoral thesis of Laura Santoso and was presented at the 49th Symposium of the Society for Histochemistry September 26–29, 2007 Freiburg im Breisgau, Germany

Udo Jeschke, Department of Obstetrics and Gynecology – Maistrasse, Ludwig-Maximilians University, Maistrasse 11, D-80337 Munich, Germany.
E-mail: udo.jeschke@med.uni-muenchen.de

Abstract

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.

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