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Identification of novel genetic markers associated with clinical phenotypes of systemic sclerosis through a genome-wide association strategy.
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Polymorphisms in the interleukin 4, interleukin 13 and corresponding receptor genes are not associated with systemic sclerosis and do not influence gene expression
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Analysis of the influence of PTPN22 gene polymorphisms in systemic sclerosis
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Variants of PBEF predispose to systemic sclerosis and pulmonary arterial hypertension development
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A replication study confirms the association of TNFSF4 (OX40L) polymorphisms with systemic sclerosis in a large European cohort
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Identification of novel genetic markers associated with clinical phenotypes of systemic sclerosis through a genome-wide association strategy
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Identification of Novel Genetic Markers Associated with Clinical Phenotypes of Systemic Sclerosis through a Genome-Wide Association Strategy
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In: PLoS Genetics, 14-07-2011 (2011)
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Analysis of the influence of PTPN22 gene polymorphisms in systemic sclerosis
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Identification of novel genetic markers associated with the clinical phenotypes of systemic sclerosis through a genome wide association strategy
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BASE
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Analysis of the influence of PTPN22 gene polymorphisms in systemic sclerosis
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BASE
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Variants of PBEF predispose to systemic sclerosis and pulmonary arterial hypertension development
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BASE
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Polymorphisms in the interleukin 4, interleukin 13 and corresponding receptor genes are not associated with Systemic Sclerosis and do not influence gene expression
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The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype
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The STAT4 gene influences the genetic predisposition to systemic sclerosis phenotype
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A large multicentre analysis of CTGF -945 promoter polymorphism does not confirm association with systemic sclerosis susceptibility or phenotype
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The interleukin 23 receptor gene does not confer risk to systemic sclerosis and is not associated with systemic sclerosis disease phenotype
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The Interleukin 23 Receptor gene does not confer risk to systemic sclerosis and is not associated with SSc disease phenotype
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Rueda, B; Broen, J; Torres, O; Simeon, C; Ortega-Centeno, N; Schrijvenaars, M MVAP; Vonk, M C; Fonollosa, V; van den Hoogen, F HJ; Coenen, M JH; Sanchez-Román, J; Aguirre-Zamorano, M A; García-Portales, R; Pros, A; Camps, M T; Gonzalez-Gay, M; Martin, J; Radstake, T RDJ. - : BMJ Publishing Group Ltd, 2008
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Abstract:
Objective: Multiple studies indicate the role of the IL-17/IL-23 axis in autoimmune diseases including systemic sclerosis (SSc). The aim of the current study was to investigate the possible implication of the IL23R gene in SSc susceptibility and/or clinical phenotype. Methods: An initial case-control study in 143 Dutch SSc patients and geographically matched healthy individuals (n = 246) was carried out and followed by a replication study in a cohort of 365 Spanish SSc patients and 515 healthy individuals. Seven single nucleotide polymorphisms (SNPs) spanning the IL23R gene were selected and genotyped using a Taqman assay. Results: Using a Dutch cohort of SSc patients and controls we observed an association between two (rs11209032, rs1495965) of the seven tested SNPs and disease susceptibility (allelic p values: P=0.02 and P=0.01 respectively). However, a replication study in an independent Spanish cohort did not confirm these findings and reveal no association of any of the IL23R tested SNP with disease susceptibility or clinical phenotype. Similarly, a meta-analysis considering both populations did not reveal any significant association. In addition, no association was observed between IL23R genetic variants and SSc clinical phenotypes. Conclusions: Our results suggest that the IL23R gene is not associated with SSc susceptibility or clinical phenotype.
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Keyword:
Concise Report
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URL: https://doi.org/10.1136/ard.2008.096719 http://ard.bmj.com/cgi/content/short/ard.2008.096719v1
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A large multicenter analysis of CTGF -945 promoter polymorphism does not confirm association with Systemic Sclerosis susceptibility or phenotype
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A large multicenter analysis of CTGF -945 promoter polymorphism does not confirm association with Systemic Sclerosis susceptibility or phenotype
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