B F Barrier1, B S Kendall, C E Ryan, K L Sharpe-Timms. 1. Department of Obstetrics, Gynecology and Women's Health, Division of Reproductive and Perinatal Research, University of Missouri-Columbia, Missouri 65212, USA. barrierb@health.missouri.edu
Abstract
BACKGROUND: HLA-G is a major histocompatability antigen with documented immune-regulatory function. Various epithelial cancers and tissue allografts have been noted to express HLA-G, which is postulated to aid in their escape from immunosurveillance. We evaluated peritoneal endometriosis and eutopic endometrium for the expression of HLA-G protein and gene transcript. METHODS: Two experiments were performed: (i) archived tissue blocks from peritoneal endometriotic lesions (n = 15) and eutopic endometrium (n = 12) were evaluated for extent of protein immunostaining, and (ii) eutopic endometrial biopsies from women without (n = 17) and with (n = 24) endometriosis, and peritoneal endometriotic lesions (n = 14) were evaluated for presence of RNA transcript by in situ hybridization. RESULTS: HLA-G protein localized in the glandular epithelium of 14 of 15 (93.3%) peritoneal endometriotic lesions, but not in stromal cells. HLA-G protein staining was absent in endometrial biopsies (n = 12). HLA-G gene transcript localized to the glandular epithelium in 13 of 14 (92.8%) peritoneal endometriotic lesions. HLA-G transcript was never observed in eutopic endometrium, regardless of cycle stage or whether from women with (n = 24) or without (n = 18) endometriosis. CONCLUSIONS: HLA-G is expressed by endometriotic glandular epithelium but not by eutopic endometrium under normal conditions. Differential expression of HLA-G suggests that peritoneal inflammation or cellular stress may up-regulate mechanisms to promote ectopic endometrial survival.
BACKGROUND:HLA-G is a major histocompatability antigen with documented immune-regulatory function. Various epithelial cancers and tissue allografts have been noted to express HLA-G, which is postulated to aid in their escape from immunosurveillance. We evaluated peritoneal endometriosis and eutopic endometrium for the expression of HLA-G protein and gene transcript. METHODS: Two experiments were performed: (i) archived tissue blocks from peritoneal endometriotic lesions (n = 15) and eutopic endometrium (n = 12) were evaluated for extent of protein immunostaining, and (ii) eutopic endometrial biopsies from women without (n = 17) and with (n = 24) endometriosis, and peritoneal endometriotic lesions (n = 14) were evaluated for presence of RNA transcript by in situ hybridization. RESULTS:HLA-G protein localized in the glandular epithelium of 14 of 15 (93.3%) peritoneal endometriotic lesions, but not in stromal cells. HLA-G protein staining was absent in endometrial biopsies (n = 12). HLA-G gene transcript localized to the glandular epithelium in 13 of 14 (92.8%) peritoneal endometriotic lesions. HLA-G transcript was never observed in eutopic endometrium, regardless of cycle stage or whether from women with (n = 24) or without (n = 18) endometriosis. CONCLUSIONS:HLA-G is expressed by endometriotic glandular epithelium but not by eutopic endometrium under normal conditions. Differential expression of HLA-G suggests that peritoneal inflammation or cellular stress may up-regulate mechanisms to promote ectopic endometrial survival.
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