title: Distribution and maturity of dendritic cells in diseases of insufficient placentation.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  Our data suggest a participation of DC-mediated immunological mechanisms in HELLP syndrome.
authors.affiliation: Department of Obstetrics and Gynecology - Maistrasse, Ludwig-Maximilians University, Munich, Germany.
authors.forename: Christoph
authors.initials: C
authors.lastname: Scholz
authors.forename: Bettina
authors.initials: B
authors.lastname: Toth
authors.forename: Laura
authors.initials: L
authors.lastname: Santoso
authors.forename: Christina
authors.initials: C
authors.lastname: Kuhn
authors.forename: Maximilian
authors.initials: M
authors.lastname: Franz
authors.forename: Doris
authors.initials: D
authors.lastname: Mayr
authors.forename: Udo
authors.initials: U
authors.lastname: Jeschke
authors.forename: Klaus
authors.initials: K
authors.lastname: Friese
authors.forename: Barbara
authors.initials: B
authors.lastname: Schiessl
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D003656:Decidua / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D005260:Female; D005317:Fetal Growth Retardation / Q000276:immunology* / Q000378:metabolism; D017359:HELLP Syndrome / Q000276:immunology* / Q000378:metabolism*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type / Q000378:metabolism; D051907:Lysosomal Membrane Proteins / Q000378:metabolism; D015778:Minor Histocompatibility Antigens; D010929:Placentation; D011225:Pre-Eclampsia / Q000276:immunology* / Q000378:metabolism; D011247:Pregnancy; D011956:Receptors, Cell Surface / Q000378:metabolism; D040262:Receptors, Vascular Endothelial Growth Factor / Q000378:metabolism; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin
chemical_list: D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D037181:Lectins, C-Type; D051907:Lysosomal Membrane Proteins; D015778:Minor Histocompatibility Antigens; D011956:Receptors, Cell Surface; D040262:Receptors, Vascular Endothelial Growth Factor; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin; C093569:DEC-205 receptor