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Polymorphisms in the CTLA-4 Gene and Rheumatoid Arthritis Susceptibility: a Meta-analysis

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Journal J Clin Immunol
Publisher Springer
Date 2012 Feb 23
PMID 22354566
Citations 12
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Abstract

Introduction: The +49A/G polymorphism and CT60 polymorphism in the CTLA-4 gene have been extensively examined for the association with rheumatoid arthritis (RA); however, results of different studies have been inconclusive. The aim of this study is to comprehensively evaluate the genetic risks of +49A/G and CT60 polymorphisms in the CTLA-4 gene for RA.

Methods: A meta-analysis was carried out to analyze the association of +49A/G and CT60 polymorphisms with RA risk.

Results: A total of 30 case-control studies in 20 articles were included in this meta-analysis. The results indicated that the variant G allele carriers (GG + GA) of +49A/G polymorphism had an 18% increased risk of RA when compared with the homozygote AA (odds ratio (OR) = 1.18, 95% confidence interval (CI): 1.04-1.34 for GG + AG vs. AA). In addition, the variant CT60 A allele carriers of CT60 polymorphism had a 14% decreased risk of RA when compared with the homozygote GG (OR = 0.86, 95%CI = 0.78-0.95 for AA + AG vs. GG). In the subgroup analysis by ethnicity, significant elevated RA risks were associated with +49G allele carriers in Asians, but not in Europeans. However, for CT60 polymorphism, significant decreased RA risks were associated with CT60 A allele carriers in Europeans, but not in Asians.

Conclusions: This meta-analysis suggested that the +49A/G and CT60 polymorphisms in the CTLA-4 gene may be risk factors for RA.

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References
1.
Tsukahara S, Iwamoto T, Ikari K, Inoue E, Tomatsu T, Hara M . CTLA-4 CT60 polymorphism is not an independent genetic risk marker of rheumatoid arthritis in a Japanese population. Ann Rheum Dis. 2008; 67(3):428-9. DOI: 10.1136/ard.2007.079186. View

2.
Barton A, Myerscough A, John S, Ollier W, Worthington J . A single nucleotide polymorphism in exon 1 of cytotoxic T-lymphocyte-associated-4 (CTLA-4) is not associated with rheumatoid arthritis. Rheumatology (Oxford). 2000; 39(1):63-6. DOI: 10.1093/rheumatology/39.1.63. View

3.
Kochi Y, Thabet M, Suzuki A, Okada Y, Daha N, Toes R . PADI4 polymorphism predisposes male smokers to rheumatoid arthritis. Ann Rheum Dis. 2010; 70(3):512-5. DOI: 10.1136/ard.2010.130526. View

4.
McCoy K, Le Gros G . The role of CTLA-4 in the regulation of T cell immune responses. Immunol Cell Biol. 1999; 77(1):1-10. DOI: 10.1046/j.1440-1711.1999.00795.x. View

5.
Orozco G, Torres B, Nunez-Roldan A, Gonzalez-Escribano M, Martin J . Cytotoxic T-lymphocyte antigen-4-CT60 polymorphism in rheumatoid arthritis. Tissue Antigens. 2004; 64(6):667-70. DOI: 10.1111/j.1399-0039.2004.00318.x. View