Skip Navigation



Mol. Hum. Reprod. Advance Access published online on December 22, 2005

Molecular Human Reproduction, doi:10.1093/molehr/gah225
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow All Versions of this Article:
11/10/745    most recent
gah225v1
Right arrow Alert me when this article is cited
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 Vigano’, P.
Right arrow Articles by Di Blasio, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vigano’, P.
Right arrow Articles by Di Blasio, A. M.
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@oupjournals.org
Received July 5, 2005
Revised July 29, 2005
Accepted August 15, 2005

Article

Variants of the CTLA4 gene that segregate with autoimmune diseases are not associated with endometriosis

Paola Vigano’ 1, Debora Lattuada 1, Edgardo Somigliana 1, Annalisa Abbiati 1, Massimo Candiani 1, and Anna Maria Di Blasio 2 *

1 Department of Obstetrics, Gynaecology and Neonatology, ‘Fondazione Policlinico-Mangiagalli-Regina Elena’ Hospital, University of Milano, Milan, Italy
2 Molecular Biology Laboratory Istituto Auxologico Italiano, Milan, Italy

* To whom correspondence should be addressed.
Anna Maria Di Blasio, E-mail: a.diblasio{at}auxologico.it


   Abstract

An autoimmune etiology has been suggested for endometriosis mostly on the basis of an increased prevalence of autoimmune diseases in affected women. Cytotoxic T lymphocyte antigen (CTLA) 4 gene is recognized as a primary determinant for autoim-munity since specific polymorphisms have been associated with predisposition to most autoimmune disorders. This study was aimed to evaluate whether two variants of CTLA4 gene might be associated with endometriosis in an Italian population. We examined the +49A/G polymorphism and the CT60A/G dimorphism in n = 146 endometriosis subjects classified according to Holt and Weiss criteria. Controls were represented by n = 165 women without laparoscopic evidence of the disease. We found no statistically significant difference in the genotype frequencies between women with and without endometriosis. The proportion of the mutant G allele of the +49A/G polymorphism in the former and in the latter group resulted 34 and 30%, respectively. The proportion of the susceptible G allele of the CT60 A/G dimorphism resulted 51% in both groups. No association was demonstrated between the polymorphisms and the clinical forms of the disease and no susceptibility haplotypes were found. These findings suggest that endometriosis aetiology is not primarily associated with the development of CTLA4-linked autoimmunity.

Keywords: Autoimmune, CTLA4, endometriosis, genetics, polymorphism.
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 Reprod UpdateHome page
C.B. Tempfer, M. Simoni, B. Destenaves, and B.C.J.M. Fauser
Functional genetic polymorphisms and female reproductive disorders: Part II--endometriosis
Hum. Reprod. Update, January 1, 2009; 15(1): 97 - 118.
[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.