title: Killer inhibitory receptor CD158a overexpression among natural killer cells in women with endometriosis is undiminished by laparoscopic surgery and gonadotropin releasing hormone agonist treatment.
abstract: OBJECTIVE
  Natural killer (NK) dysfunction is considered to contribute to the pathogenesis of endometriosis. In this study, we investigated the host immune response to endometriosis in terms of killer inhibitory receptor (KIR) expression by NK cells.
  
  
  METHODS
  We compared cells from Japanese women laparoscopically diagnosed with endometriosis and treated with laparoscopic surgery (n = 98), 1 month after laparoscopic surgery (n = 36), and 12 weeks after gonadotropin releasing hormone agonist (GnRHa) treatment (n = 18) to cells from 104 women with other laparoscopic diagnoses. KIR expression by NK cells was assessed in peripheral blood and peritoneal fluid samples by flow cytometry.
  
  
  RESULTS
  In women with endometriosis, the percentage of CD158a-expressing cells among CD16-expressing NK (CD158a(+)NK) cells in both peritoneal fluid and peripheral blood was significantly higher than in control subjects. No significant differences in proportion of CD158a(+)NK cells were identified between peripheral blood NK cells sampled before and 1 month after laparoscopic surgery, or 12 weeks after initiating GnRHa treatment.
  
  
  CONCLUSIONS
  Increased percentage of CD158a(+)NK cells in peripheral blood from women with endometriosis was undiminished by laparoscopic surgery and GnRHa treatment; the persistence of CD158a(+)NK cell excess is probably related to NK cell suppression in endometriosis. This overexpression may represent a risk factor for development of endometriosis and its recurrence after treatments.
authors.affiliation: Department Obstetrics and Gynecology, Kochi Medical School Oko, Nankoku, Kochi, Japan. maedan@med.kochi-u.ac.jp
authors.forename: Nagamasa
authors.initials: N
authors.lastname: Maeda
authors.forename: Chiaki
authors.initials: C
authors.lastname: Izumiya
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Kusum
authors.forename: Takayuki
authors.initials: T
authors.lastname: Masumoto
authors.forename: Chika
authors.initials: C
authors.lastname: Yamashita
authors.forename: Yorito
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: Hiroyoshi
authors.initials: H
authors.lastname: Oguri
authors.forename: Takao
authors.initials: T
authors.lastname: Fukaya
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D001202:Ascitic Fluid / Q000737:chemistry / Q000166:cytology; D002452:Cell Count; D003627:Data Interpretation, Statistical; D018450:Disease Progression; D004715:Endometriosis / Q000276:immunology* / Q000378:metabolism / Q000628:therapy; D005260:Female; D005434:Flow Cytometry; D005498:Follicular Phase / Q000378:metabolism; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists* / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007694:Killer Cells, Natural / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D010535:Laparoscopy; D037181:Lectins, C-Type / Q000032:analysis; D007963:Leukocytes, Mononuclear / Q000737:chemistry; D008183:Luteal Phase / Q000378:metabolism; D008875:Middle Aged; D051920:NK Cell Lectin-Like Receptor Subfamily D; D017452:Receptors, IgG / Q000032:analysis; D011971:Receptors, Immunologic / Q000032:analysis / Q000378:metabolism*; D054340:Receptors, KIR; D054342:Receptors, KIR2DL1
chemical_list: D015703:Antigens, CD; D037181:Lectins, C-Type; D051920:NK Cell Lectin-Like Receptor Subfamily D; D017452:Receptors, IgG; D011971:Receptors, Immunologic; D054340:Receptors, KIR; D054342:Receptors, KIR2DL1; D007987:Gonadotropin-Releasing Hormone; C083781:LHRH, Ala(6)-Gly(10)-ethylamide-