title: Peritoneal cellular immunity and endometriosis.
abstract: OBJECTIVE
  An immunologic basis has long been considered to be very important in the pathogenesis of endometriosis. Interactions of the peritoneal cells, which comprise macrophages, B cells, T cells, natural killer (NK) cells, and retrograde endometrial cells, are critical, but remain controversial, for exploring the pathogenesis of endometriosis.
  
  
  METHODS
  Accumulated data from the literature were reviewed, and our data were analyzed.
  
  
  RESULTS
  The data show that peritoneal macrophages are activated by the recurrent reflux of menstrual shedding. Humoral and local endometrial autoantibodies are detected in patients with endometriosis, but B cells are not quantitatively increased. There is decreased NK cell activity in the peritoneal cavity and peripheral blood, and this decreased activity may be related to the failure to clear out the ectopic endometrial tissue. Peritoneal T cells are predominant by Th1 inflammatory cells, and these cells are impaired because of a decrease in activation (especially HLA-DR+CD4+CD3+ population) and in the production of interleukin-2. Inflammatory cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-alpha are elevated in the peritoneal fluid of women with endometriosis.
  
  
  CONCLUSIONS
  The peritoneal NK and T lymphocytes are suppressed in women with endometriosis, but whether these immunologic deviations are the cause or the result of endometriosis is still unclear. Further studies are required to determine what role immunologic factors play in the pathophysiology of endometriosis.
authors.affiliation: Department of Obstetrics and Gynecology, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China. HNHO@HA.MC.NTU.EDU.TW
authors.forename: H N
authors.initials: HN
authors.lastname: Ho
authors.forename: M Y
authors.initials: MY
authors.lastname: Wu
authors.forename: Y S
authors.initials: YS
authors.lastname: Yang
mesh_terms: D001402:B-Lymphocytes / Q000502:physiology; D004715:Endometriosis / Q000209:etiology / Q000276:immunology*; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007694:Killer Cells, Natural / Q000502:physiology; D017737:Macrophages, Peritoneal / Q000502:physiology; D010537:Peritoneum / Q000276:immunology*; D013601:T-Lymphocytes / Q000502:physiology