Hum. Reprod. Advance Access originally published online on November 25, 2005
Human Reproduction 2006 21(4):864-869; doi:10.1093/humrep/dei408
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HLA-G is expressed by the glandular epithelium of peritoneal endometriosis but not in eutopic endometrium
1 Department of Obstetrics, Gynecology and Women’s Health, Division of Reproductive and Perinatal Research, University of Missouri–Columbia, Missouri and 2 Department of Pathology, Wilford Hall Medical Center, Lackland A.F.B., Texas, USA
3 To whom correspondence should be addressed at: Department of Obstetrics, Gynecology and Women’s Health, 1 Hospital Drive, N 625 HSC, University of Missouri–Columbia, Columbia, MO 65212. E-mail: barrierb{at}health.missouri.edu
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.
Key words: endometriosis/endometrium/HLA-G/immunology/inflammation