title: Role of major histocompatibility complex class I expression and natural killer-like T cells in the genetic control of endometriosis.
abstract: OBJECTIVE
  To evaluate whether the expression of human leukocyte antigen (HLA) class I on eutopic and ectopic endometrial cells modify the susceptibility to lysis mediated by lymphocytes.
  
  
  METHODS
  Evaluation of T lymphocyte cytotoxic activity and HLA class I expression on endometrial cells.
  
  
  METHODS
  Subjects were recruited at laparoscopy.
  
  
  METHODS
  Patients with endometriosis (n = 7). Healthy women as controls (n = 10).
  
  
  METHODS
  Human leukocyte antigen class I molecule analysis of endometrial cells was carried out by immunofluorescence and flow cytometry. Phenotyping of T lymphocytes was performed to analyze T-cell subsets. Cytotoxicity was performed to determine cytolytic activity against endometrial cells.
  
  
  RESULTS
  In vitro culture of endometrial cells down-regulates the expression of HLA class I molecules and enhances the susceptibility to lysis mediated by natural killer (NK)-like T lymphocytes. Cytolytic T-cell clones, expressing the CD94 antigen, are inhibited by the HLA-B7 allele on endometrial cells. Ectopic endometrial cells modulate the expression of HLA class I molecules.
  
  
  CONCLUSIONS
  The resistance to lysis of endometrial cells is related to expression of surface HLA class I molecules, which send a negative signal for lysis mediated by NK-like T lymphocytes. The HLA-B7 allele inhibits the cytotoxic activity, suggesting that the growth of ectopic endometrial cells might be under a genetic control.
authors.affiliation: Servizio di Citometria, Istituto Nazionale per la Ricerca sul Cancro, Genova, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Semino
authors.forename: A
authors.initials: A
authors.lastname: Semino
authors.forename: G
authors.initials: G
authors.lastname: Pietra
authors.forename: M C
authors.initials: MC
authors.lastname: Mingari
authors.forename: S
authors.initials: S
authors.lastname: Barocci
authors.forename: P L
authors.initials: PL
authors.lastname: Venturini
authors.forename: N
authors.initials: N
authors.lastname: Ragni
authors.forename: G
authors.initials: G
authors.lastname: Melioli
mesh_terms: D000483:Alleles; D002478:Cells, Cultured; D015536:Down-Regulation; D004715:Endometriosis / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology*; D004717:Endometrium / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D019084:Fluorescent Antibody Technique, Indirect; D005786:Gene Expression Regulation; D005805:Genes, MHC Class I; D015793:HLA-B7 Antigen / Q000032:analysis / Q000235:genetics; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D007694:Killer Cells, Natural / Q000276:immunology / Q000473:pathology / Q000502:physiology*; D010641:Phenotype; D013602:T-Lymphocytes, Cytotoxic / Q000473:pathology / Q000502:physiology
chemical_list: D015793:HLA-B7 Antigen; D015395:Histocompatibility Antigens Class I; D007371:Interferon-gamma