title: Lymphocyte subsets and autoantibodies in pregnancies complicated by placental disorders.
abstract: OBJECTIVE
  The survival of the fetoplacental unit might partly depend on down-regulation of rejection reactions. Pathological maternal cellular immune response mechanisms could therefore be of pathogenic importance in pregnancies complicated by placental disorders.
  
  
  METHODS
  A flow-cytometric analysis of T-cell subsets and B-cell, as well as serological tests for anticardiolipin antibodies (aCL), antinuclear antibodies (ANA), and rheumatoid factor (RF) were done on 90 women with complicated pregnancies. The results were compared with that of nonpregnant women (n = 5), and normal pregnant women (n = 5) in the third trimester.
  
  
  RESULTS
  Two women, suffering from severe preeclampsia and eclampsia respectively, had aCL on 12 and 13 units, respectively. ANA occurred in 11 patients with moderate and severe preeclampsia and intrauterine growth retardation. All women had negative RF tests. Within the CD4 T-helper subpopulations, the proportion of suppressor/inducer T-cell population (CD4+CD45RA+) significantly increased, while the memory and helper/inducer T-cells (CD4+CD45RO+ and CD4+CD29+) significantly decreased during normal pregnancy compared to nonpregnant controls. This deviation of CD4 subpopulations was not found, or was less pronounced, in complicated pregnancies. The proportion of cytotoxic T cells (CD8+S6F1+) was significantly reduced during normal pregnancy. This reduction was less pronounced in complicated pregnancies.
  
  
  CONCLUSIONS
  Systemic immunological deviations toward suppression or decreased activity of the immunological response as seen in normal pregnancies, was not observed in preeclampsia, intrauterine growth retardation, intrauterine fetal death, and abruptio placentae. This lack of suppression or increased T-cell activity may have a primary pathogenic role in some women with a complicated pregnancy, or it may be secondary to the placental disorders.
authors.affiliation: Department of Obstetrics and Gynaecology, University of Linköping, Sweden.
authors.forename: L
authors.initials: L
authors.lastname: Matthiesen
authors.forename: G
authors.initials: G
authors.lastname: Berg
authors.forename: J
authors.initials: J
authors.lastname: Ernerudh
authors.forename: T
authors.initials: T
authors.lastname: Skogh
mesh_terms: D000037:Abruptio Placentae / Q000276:immunology; D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000097:blood; D001323:Autoantibodies / Q000276:immunology*; D004461:Eclampsia / Q000276:immunology; D005260:Female; D005313:Fetal Death / Q000276:immunology; D005317:Fetal Growth Retardation / Q000276:immunology; D005434:Flow Cytometry; D006801:Humans; D007108:Immune Tolerance; D016130:Immunophenotyping; D018655:Lymphocyte Count; D016131:Lymphocyte Subsets; D008875:Middle Aged; D010922:Placenta Diseases / Q000276:immunology*; D011225:Pre-Eclampsia / Q000276:immunology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000276:immunology*; D011263:Pregnancy Trimester, Third; D012217:Rheumatoid Factor / Q000097:blood; D013927:Thrombosis / Q000276:immunology
chemical_list: D017153:Antibodies, Anticardiolipin; D001323:Autoantibodies; D012217:Rheumatoid Factor