TNF-α Gene Promoter -238G>A and -308G>A Polymorphisms Alter Risk of Psoriasis Vulgaris: A Meta-Analysis
Tumor necrosis factor-α (TNF-α) is a major proinflammatory cytokine and involved in the etiology of psoriasis. The -238G>A and -308G>A polymorphisms influence the transcription of the TNF-α gene and have been implicated in psoriasis risk. However, the results from the published studies on the...
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Published in | Journal of investigative dermatology Vol. 127; no. 8; pp. 1886 - 1892 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Danvers, MA
Elsevier Inc
01.08.2007
Nature Publishing |
Subjects | |
Online Access | Get full text |
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Summary: | Tumor necrosis factor-α (TNF-α) is a major proinflammatory cytokine and involved in the etiology of psoriasis. The -238G>A and -308G>A polymorphisms influence the transcription of the TNF-α gene and have been implicated in psoriasis risk. However, the results from the published studies on the association between TNF-α polymorphisms and psoriasis risk are conflicting. Our meta-analysis of a total of 997 psoriasis cases and 943 control subjects from eight published case–control studies for the -238G>A polymorphism and of 1,156 psoriasis cases and 1,083 control subjects from 10 published case–control studies for the -308G>A polymorphism showed that a significantly increased risk was associated with the variant GA+AA genotypes of -238G>A, compared with the GG genotype (odds ratio (OR) 2.60, 95% confidence interval (95% CI) 1.48–4.56), whereas a significantly reduced psoriasis risk was associated with the variant GA+AA genotypes of the -308G>A compared with the GG genotype (OR 0.57, 95% CI 0.45–0.71). Our findings suggest that TNF-α -238G>A and -308G>A polymorphisms might be used as biomarkers for psoriasis risk prediction. A single larger study with thousands of subjects and biochemical and biological characterization is warranted to evaluate further the role of -238G>A and -308G>A polymorphisms and psoriasis risk in a population of various ethnicities. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 0022-202X 1523-1747 1523-1747 |
DOI: | 10.1038/sj.jid.5700822 |