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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.


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