Skip Navigation

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (9)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Coakley, G.
Right arrow Articles by Lanchbury, J. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Coakley, G.
Right arrow Articles by Lanchbury, J. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Rheumatology 1999; 38: 883-886
© 1999 British Society for Rheumatology

A Fas promoter polymorphism at position -670 in the enhancer region does not confer susceptibility to Felty's and large granular lymphocyte syndromes

G. Coakley1,2, N. Manolios3, T. P. Loughran, Jr4, G. S. Panayi2 and J. S. Lanchbury1

1 Departments of Molecular Immunogenetics and
2 Rheumatology, 5th Floor, Thomas Guy House, Guy's, King's and St Thomas' School of Medicine, Guy's Hospital, London SE1 9RT, UK,
3 Department of Rheumatology, Westmead Hospital, NSW 2145, Australia and
4 H. Lee Moffitt Cancer Center and Veteran's Administration Hospital, Departments of Medicine and Microbiology/Immunology, University of South Florida, 12902 Magnolia Drive, Suite 3157, Tampa, FL, USA

Correspondence to: J. S. Lanchbury, Molecular Immunogenetics, 5th Floor, Thomas Guy House, Guy's, King's and St Thomas' School of Medicine, Guy's Hospital, London SE1 9RT, UK.

Objective. We examined whether there are associations between a polymorphism in the Fas promoter, recently found to be associated with rheumatoid arthritis (RA), and Felty's syndrome or large granular lymphocyte (LGL) leukaemia.

Methods. Thirty-five patients with Felty's were studied, along with 18 patients with LGL syndrome and arthritis, 17 patients with LGL syndrome but no arthritis, and 128 controls. The polymorphism was typed by polymerase chain reaction followed by digestion with the restriction enzyme MvaI.

Results. No significant difference was found in genotype or allele frequencies between the groups.

Conclusion. This promoter polymorphism is not a significant risk factor responsible for the LGL expansions seen in Felty's and LGL syndromes. Abnormal, constitutive expression of Fas ligand may be more relevant to the aetiology of these diseases.

KEY WORDS: Felty's syndrome, Large granular lymphocyte, Fas, Polymorphism, Rheumatoid arthritis, Fas ligand.


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
 Rheumatology (Oxford)Home page
G. Coakley, D. Brooks, M. Iqbal, E. Kondeatis, R. Vaughan, T. P. Loughran Jr, G. S. Panayi, and J. S. Lanchbury
Major histocompatility complex haplotypic associations in Felty's syndrome and large granular lymphocyte syndrome are secondary to allelic association with HLA-DRB1 *0401
Rheumatology, April 1, 2000; 39(4): 393 - 398.
[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.