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

Objective: The immunological mechanisms that support persistence and prolif eration of ectopic endometrial implants within the peritoneal cavity of wom en with endometriasis are unknown. Inhibition of natural killer (NK) and cy totoxic T-cell function has been proposed as a mechanism. We tested the hyp othesis that expression of a nonclassical major histocompatibility antigen, HLA-G, might explain the local immunosuppression associated with ectopic e ndometrium. Design: Nested case-control study of women with and without laparoscopic ev idence 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 laparos copic evidence of endometriosis were tested for the presence of HLA-G prote in. Endometriosis and normal endometrial biopsies from four patients were u sed 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, tissu e, and cell cultures determined by immunoblotting with a specific monoclona l antibody. Result(s): HLA-G protein was not detectable in peritoneal fluid specimens o f 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 Amer ican Society far Reproductive Medicine.)