title: Changes in T-cell regulation of responses to self antigens in women with pelvic endometriosis.
abstract: OBJECTIVE
  To study autoimmune aspects of endometriosis.
  
  
  METHODS
  Lymphoblast transformation and hemolytic plaque formation were used to assess specific T- and B-cell activity against endometrial antigens.
  
  
  METHODS
  Military teaching hospital.
  
  
  METHODS
  Ninety-four healthy women of reproductive age undergoing diagnostic laparoscopy as part of an evaluation for infertility or chronic pelvalgia were accordingly grouped into those with normal pelvic peritoneum (20), mild endometriosis (50), and severe endometriosis (24).
  
  
  METHODS
  The study assessed the proliferative and humoral responses of lymphocytes from women with and without endometriosis to endometrial antigens and quantified the number of B-cell precursors, T-helper cells, and T-suppressor cells to these antigens.
  
  
  RESULTS
  Unfractionated endometrial antigens were similarly blastogenic for lymphocytes from women with and without endometriosis. Despite equivalent numbers of B-cell precursors to these antigens, antiendometrial antibody responsiveness appears to have increased in women with mild endometriosis because of a decrease in T-suppressor cell activity and declined in women with severe endometriosis because of a further drop in T-suppressor cell activity and an increase in T-helper cell activity, as compared with women without endometriosis.
  
  
  CONCLUSIONS
  Taken together, these experiments support the possibility that pelvic endometriosis may result from a break in specific T-cell tolerance rather than nonspecific polyclonal activation of responder lymphocytes.
authors.affiliation: Department of Obstetrics and Gynecology, United States Naval Hospital, Portsmouth, Virginia.
authors.forename: D S
authors.initials: DS
authors.lastname: Cunningham
authors.forename: K A
authors.initials: KA
authors.lastname: Hansen
authors.forename: C C
authors.initials: CC
authors.lastname: Coddington
mesh_terms: D001323:Autoantibodies / Q000502:physiology*; D001324:Autoantigens / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology / Q000502:physiology; D001706:Biopsy; D004715:Endometriosis / Q000453:epidemiology / Q000276:immunology* / Q000503:physiopathology; D004717:Endometrium / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D012307:Risk Factors; D013601:T-Lymphocytes / Q000276:immunology / Q000502:physiology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000502:physiology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000502:physiology
chemical_list: D001323:Autoantibodies; D001324:Autoantigens