title: Maternal-fetal HLA-DR relationships and pregnancy-induced hypertension.
abstract: OBJECTIVE
  Some studies have found an increased prevalence of pregnancy-induced hypertension among women sharing HLA antigens with their spouses or fetuses, thus supporting the hypothesis that maternal sensitization to fetal HLA alloantigens reduces the risk for pregnancy-induced hypertension. However, not all studies have confirmed these findings. No investigators have examined the four different types of maternal-fetal HLA relationships in their studies of pregnancy-induced hypertension. Our goal was to examine such associations to test further the HLA-allosensitization hypothesis.
  
  
  METHODS
  We conducted a cohort study of pregnancy-induced hypertension among 683 nulliparous women. Women and their neonates were typed for HLA-A, -B, -DR, and -DQ antigens using serologic techniques to establish maternal-fetal relationships.
  
  
  RESULTS
  We found an increased prevalence of pregnancy-induced hypertension when the fetus, but not the mother, was potentially exposed to HLA-DR alloantigens (maternal allogenicity) compared with the other three conditions combined (P < .003). Controlling for confounding factors, the increased prevalence of pregnancy-induced hypertension persisted in situations of maternal HLA-DR allogenicity (P < .007).
  
  
  CONCLUSIONS
  Based upon our observations and other immunologic studies of pregnancy-induced hypertensive and uncomplicated pregnancies, we conclude that a maternal humoral response against fetal anti-HLA-DR immunoglobulin (IgG) antibody may influence the development of pregnancy-induced hypertension. This could occur when an immunocompetent fetus is exposed to maternal HLA-DR alloantigens, maternal exposure to fetal HLA-DR alloantigens alloantigens, maternal exposure to fetal HLA-DR alloantigens is not possible, and fetal IgG antibody bears paternally inherited markers allogeneic to the mother.
authors.affiliation: Department of Pediatrics, College of Medicine, University of South Alabama, Mobile.
authors.forename: C
authors.initials: C
authors.lastname: Hoff
authors.forename: K
authors.initials: K
authors.lastname: Peevy
authors.forename: K
authors.initials: K
authors.lastname: Giattina
authors.forename: J A
authors.initials: JA
authors.lastname: Spinnato
authors.forename: R D
authors.initials: RD
authors.lastname: Peterson
mesh_terms: D004461:Eclampsia / Q000097:blood / Q000453:epidemiology / Q000276:immunology*; D005260:Female; D005312:Fetal Blood / Q000276:immunology*; D015234:HLA-A Antigens / Q000097:blood; D015235:HLA-B Antigens / Q000097:blood; D006683:HLA-DQ Antigens / Q000097:blood; D006684:HLA-DR Antigens / Q000097:blood*; D006801:Humans; D007231:Infant, Newborn; D011225:Pre-Eclampsia / Q000097:blood / Q000453:epidemiology / Q000276:immunology; D011247:Pregnancy; D015995:Prevalence
chemical_list: D015234:HLA-A Antigens; D015235:HLA-B Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens