Skip Navigation



Hum. Reprod. Advance Access published online on November 25, 2005
Human Reproduction, doi:10.1093/humrep/dei408
This Article
Right arrow FREE Full Text (PDF ) Freely available
Right arrow All Versions of this Article:
21/4/864    most recent
dei408v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Barrier, B.F.
Right arrow Articles by Sharpe-Timms, K.L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Barrier, B.F.
Right arrow Articles by Sharpe-Timms, K.L.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received August 30, 2005
Revised October 17, 2005
Accepted October 27, 2005

Article

HLA-G is expressed by the glandular epithelium of peritoneal endometriosis but not in eutopic endometrium

B.F. Barrier 1 *, B.S. Kendall 2, C.E. Ryan 1, and K.L. Sharpe-Timms 1

1 Department of Obstetrics, Gynecology and Women’s Health, Division of Reproductive and Perinatal Research, University of Missouri-Columbia, Missouri
2 Department of Pathology, Wilford Hall Medical Center, Lackland A.F.B., Texas, USA

* To whom correspondence should be addressed.
B.F. Barrier, E-mail: barrierb{at}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.

Keywords: endometriosis/endometrium/HLA-G/immunology/inflammation.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Hum ReprodHome page
C. Helige, H. Ahammer, A. Hammer, B. Huppertz, H.-G. Frank, and G. Dohr
Trophoblastic invasion in vitro and in vivo: similarities and differences
Hum. Reprod., July 11, 2008; (2008) den198v1.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.