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Rheumatology Advance Access published online on October 8, 2009
Rheumatology, doi:10.1093/rheumatology/kep280
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

CT60 and +49 polymorphisms of CTLA 4 are associated with ANCA-positive small vessel vasculitis

Lavanya Kamesh1, Joanne M. Heward2, Julie M. Williams2, Stephen C. L. Gough2, Konstantia-Maria Chavele3, Alan Salama3, Charles Pusey3, Caroline O. S. Savage2 and Lorraine Harper2

1Renal Unit, University Hospitals Birmingham NHS Foundation Trust, 2Division of Immunity and Infection, The Medical School, University of Birmingham, Birmingham and 3Renal Unit, Imperial College London, London, UK.

Correspondence to: Lorraine Harper, Division of Immunity and Infection, The Medical School, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. E-mail: l.harper{at}bham.ac.uk


  Abstract

Objective. To investigate whether single nucleotide polymorphisms (SNPs) within cytotoxic T-lymphocyte antigen-4 (CTLA-4) are associated with ANCA-associated small vessel vasculitis (SVV).

Methods. The CTLA-4 CT60 (exon 4), +49 (exon 1) and –318 (promoter region) genotypes were determined by PCR and restriction fragment length polymorphism (RFLP) in 222 white Caucasians of UK origin with SVV and 670 ethnically matched controls.

Results. The CTLA-4 exon 1 (+49) and 4 (CT60) polymorphisms are associated with SVV (+49: {chi}2 = 10.965, P = 0.004; CT60: {chi}2 = 12.017, P = 0.002). Both disease-susceptible and disease-protective haplotypes have been identified in this cohort, and their frequencies are similar in the subtypes of WG and microscopic polyangiitis.

Conclusion. This study provides further evidence that CTLA-4, a susceptibility locus for a number of common autoimmune diseases, may also be involved in the development of ANCA-associated SVV.

KEY WORDS: Polymorphisms, Vasculitis, CTLA-4

Submitted 19 May 2009; revised version accepted 31 July 2009.
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