title: Prolonged preterm rupture of fetal membranes, a consequence of an increased maternal anti-fetal T cell responsiveness.
abstract: A fetus, although semi-allogeneic, is usually accepted by the maternal immune system. However, complications, including alloresponsive mechanisms, are thought to be potentially detrimental for a successful pregnancy. Therefore, we compared allogeneic T cell responses of nonpregnant women with the response of healthy pregnant women and pregnant women who have various gestation-associated diseases. Peripheral blood mononuclear cells (PBMCs) of all three groups were stimulated with PBMCs from unrelated volunteers. Pregnant women had significantly reduced stimulation indices (SIs) compared with nonpregnant women. Exposing PBMCs from pregnant women to PBMCs of their own fetus led to a further significant decrease of SIs. Among the two groups of pregnant individuals, SIs of women with prolonged preterm rupture of fetal membranes (PPROM) were significantly higher when the maternal PBMCs were stimulated with PBMCs of their own fetus. This phenomenon could not be observed after stimulation with PBMCs from unrelated volunteers. In addition, an increased humoral immune response was assessed for women with PPROM in comparison with women with uncontrollable preterm labor. Our results revealed a strongly reduced allogeneic T cell response of PBMCs from pregnant women that was further down-regulated when PBMCs from their own fetus were used as stimulators. By contrast, data from women with PPROM suggest an increased maternal T cell response specifically toward the fetal HLA antigens.
authors.affiliation: Department of Obstetrics and Gynecology, University of Frankfurt, Germany. andrea.steinborn@med.uni-heidelberg.de
authors.forename: Andrea
authors.initials: A
authors.lastname: Steinborn
authors.forename: Edgar
authors.initials: E
authors.lastname: Schmitt
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Stein
authors.forename: Andreas
authors.initials: A
authors.lastname: Klee
authors.forename: Markus
authors.initials: M
authors.lastname: Gonser
authors.forename: Erhard
authors.initials: E
authors.lastname: Seifried
authors.forename: Christian
authors.initials: C
authors.lastname: Seidl
mesh_terms: D000328:Adult; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000473:pathology*; D005865:Gestational Age; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D007107:Immune System; D007249:Inflammation; D007963:Leukocytes, Mononuclear / Q000166:cytology; D008297:Male; D011247:Pregnancy; D013601:T-Lymphocytes / Q000276:immunology*; D013997:Time Factors
chemical_list: D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II