Histocompatibility leukocyte antigen-G is not expressed by endometriosis or endometrial tissue

Objective: The immunological mechanisms that support persistence and proliferation of ectopic endometrial implants within the peritoneal cavity of women with endometriasis are unknown. Inhibition of natural killer (NK) and cytotoxic T-cell function has been proposed as a mechanism. We tested the hypothesis that expression of a nonclassical major histocompatibility antigen, HLA-G, might explain the local immunosuppression associated with ectopic endometrium. Design: Nested case-control study of women with and without laparoscopic evidence of endometriosis. Setting: Reproductive endocrinology clinic at a university hospital. Patient(s): Peritoneal fluid specimens from 10 women with revised AFS stage I-IV endometriosis and from 10 age-matched normal controls without laparoscopic evidence of endometriosis were tested for the presence of HLA-G protein. Endometriosis and normal endometrial biopsies from four patients were used to prepare stromal cell cultures directly evaluated for HLA-G protein. Intervention(s): None. Main Outcome Measure(s): The expression of HLA-G in peritoneal fluid, tissue, and cell cultures determined by immunoblotting with a specific monoclonal antibody. Result(s): HLA-G protein was not detectable in peritoneal fluid specimens of endometriosis patients controls. Moreover, ectopic and normal endometrial tissues and stromal cells did not express HLA-G. Conclusion(s): Immune cell inhibition in endometriosis must be mediated by factors other thanKLA-G. (Fertil Steril (R) 2001;75:814-7. (C) 2001 by American Society far Reproductive Medicine.)