title: Leukocyte activation in the decidua of chromosomally normal and abnormal fetuses from women with recurrent abortion.
abstract: As part of our continuing programme to investigate immunological causes of unexplained recurrent pregnancy losses, we studied subpopulations of white blood cells and their activation status in decidua of women with a history of recurrent spontaneous abortion (RSA). We differentiated specifically between normal karyotyped male fetuses and abnormal karyotyped fetuses with trisomy 16 because trisomy 16 is not compatible with life and is thus a non-controversial cause of spontaneous miscarriage. Leukocytes were counted in paraffin-embedded decidua after immunohistological staining for CD45 (LCA), CD3, CD56, CD68, CD69 and CD25. Numbers of activated versus non-activated T lymphocytes, NK cells and macrophages were compared in decidua from women with: (i) unexplained RSA who had a normal male karyotype (n = 17) miscarriage; (ii) unexplained RSA who had a trisomy 16 (n = 21) miscarriage; and (iii) normal gestationally age-matched first trimester pregnancies following elective termination procedures (n = 20). Significantly more activated leukocytes were detected in the decidua of women with unexplained RSA who had a normal male karyotype compared to the other groups (P < 0.0001). In addition, numbers of cells comprising the major leukocyte subpopulation, CD56+ NK cells, appeared reduced in the decidua of women with unexplained RSA compared to decidua from women having elective terminations. Increased numbers of activated leukocytes in the decidua of women with a history of unexplained recurrent pregnancy loss who had a normal karyotyped pregnancy provide evidence that cellular immunity may be involved in unexplained recurrent pregnancy loss.
authors.affiliation: Fearing Laboratory and The Center for Reproductive Medicine, Department of Obstetrics, Gynecology and Reproductive Biology, Harvard Medical School, Brigham and Women's Hospital, Boston 02115, USA.
authors.forename: K C
authors.initials: KC
authors.lastname: Quack
authors.forename: N
authors.initials: N
authors.lastname: Vassiliadou
authors.forename: J
authors.initials: J
authors.lastname: Pudney
authors.forename: D J
authors.initials: DJ
authors.lastname: Anderson
authors.forename: J A
authors.initials: JA
authors.lastname: Hill
mesh_terms: D000026:Abortion, Habitual / Q000235:genetics* / Q000276:immunology* / Q000473:pathology; D000911:Antibodies, Monoclonal; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D017252:CD3 Complex / Q000032:analysis; D019002:CD56 Antigen / Q000032:analysis; D002869:Chromosome Aberrations; D002885:Chromosomes, Human, Pair 16; D003656:Decidua / Q000276:immunology* / Q000473:pathology; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007150:Immunohistochemistry; D007621:Karyotyping; D007694:Killer Cells, Natural / Q000276:immunology; D037181:Lectins, C-Type; D017493:Leukocyte Common Antigens / Q000032:analysis; D007958:Leukocyte Count; D007962:Leukocytes / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology; D014314:Trisomy; D000099192:CD69 Antigens; D000097382:CD68 Molecule
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; D019002:CD56 Antigen; D037181:Lectins, C-Type; D017493:Leukocyte Common Antigens; D015375:Receptors, Interleukin-2; D000099192:CD69 Antigens; C067980:CD68 antigen, human; D000097382:CD68 Molecule