Literature DB >> 22422496

Independent replication and meta analysis of association studies establish TNFSF4 as a susceptibility gene preferentially associated with the subset of anticentromere-positive patients with systemic sclerosis.

Baptiste Coustet1, Matthieu Bouaziz, Philippe Dieudé, Mickael Guedj, Lara Bossini-Castillo, Sandeep Agarwal, Timothy Radstake, Javier Martin, Pravitt Gourh, Muriel Elhai, Eugénie Koumakis, Jérôme Avouac, Barbara Ruiz, Maureen Mayes, Frank Arnett, Eric Hachulla, Elisabeth Diot, Jean-Luc Cracowski, Kiet Tiev, Jean Sibilia, Luc Mouthon, Camille Frances, Zahir Amoura, Patrick Carpentier, Anne Cosnes, Olivier Meyer, André Kahan, Catherine Boileau, Gilles Chiocchia, Yannick Allanore.   

Abstract

OBJECTIVE: Independent replication with large cohorts and metaanalysis of genetic associations are necessary to validate genetic susceptibility factors. The known tumor necrosis factor (ligand) superfamily, member 4 gene (TNFSF4) systemic lupus erythematosus (SLE) risk locus has been found to be associated with systemic sclerosis (SSc) in 2 studies, but with discrepancies between them for genotype-phenotype correlation. Our objective was to validate TNFSF4 association with SSc and determine the subset with the higher risk.
METHODS: Known SLE and SSc TNFSF4 susceptibility variants (rs2205960, rs1234317, rs12039904, rs10912580, and rs844648) were genotyped in 1031 patients with SSc and 1014 controls of French white ancestry. Genotype-phenotype association analysis and meta analysis of available data were performed, providing a population study of 4989 patients with SSc and 4661 controls, all of European white ancestry.
RESULTS: Allelic and genotypic associations were observed for the 5 single-nucleotide polymorphisms (SNP) with the subset of patients with SSc who are positive for anticentromere antibodies (ACA) and only a trend for association with SSc and limited cutaneous SSc. Rs2205960 exhibited the strongest allelic association in ACA+ patients with SSc [p = 0.0015; OR 1.37 (1.12-1.66)], with significant intra-cohort association when compared to patients with SSc positive for ACA. Metaanalysis confirmed overall association with SSc but also raised preferential association with the ACA+ subset and strongest effect with rs2205960 [T allele p = 0.00013; OR 1.33 (1.15-1.54) and TT genotype p = 0.00046; OR 2.02 (1.36-2.98)].
CONCLUSION: We confirm TNFSF4 as an SSc susceptibility gene and rs2205960 as a putative causal variant with preferential association in the ACA+ SSc subphenotype.

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Year:  2012        PMID: 22422496      PMCID: PMC3687343          DOI: 10.3899/jrheum.111270

Source DB:  PubMed          Journal:  J Rheumatol        ISSN: 0315-162X            Impact factor:   4.666


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