Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
11022630 | Gene | 2019 | 24 Pages |
Abstract
Psoriasis is a chronic immune-mediated disease with a complex etiology involving various genetic and immunological factors as well as environmental factors. Psoriasis is thought to be mediated by T-cells polarized to a Th17 fate. PTPN2 encodes the T-cell protein tyrosine phosphatase, which acts as a negative regulator of the JAK/STAT signaling pathways downstream of cytokines and plays a prominent role in T-cell activation, signaling and/or effector function. To evaluate the association between PTPN2 gene polymorphisms and psoriasis in the Northeastern Chinese population. A case-control study was conducted, and 398 patients with psoriasis and 397 healthy controls were genotyped for thirteen genetic polymorphisms in PTPN2. Allele analysis revealed that rs2847297, rs657555 and rs482160 polymorphisms were significantly associated with psoriasis (pâ¯=â¯0.0018, pâ¯=â¯0.0017 and pâ¯=â¯0.0086, respectively). Genotype analysis also revealed that these polymorphisms were significantly associated with psoriasis under different models (codominant, dominant and recessive models) (pâ¯<â¯0.05). In this study, three haplotypes (H1, H7 and H11) were also found to be associated with psoriasis (pâ¯=â¯0.0015, pâ¯=â¯0.0094, and pâ¯=â¯0.0124, respectively). These results indicate that PTPN2 genetic polymorphisms are associated with psoriasis in the Northeastern Chinese population.
Keywords
CNVPTPN2ORSPTPHWENGS95% CIJAK/STATHardy-Weinberg equilibriumNext-generation sequencingcopy number variationNortheastern ChinaLinkage disequilibrium95% confidence intervalsGenome-wide association studiesGWASProtein tyrosine phosphatasePsoriasisPolymorphismsjanus kinase/signal transducers and activators of transcription
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Genetics
Authors
Qingbu Mei, Chang Liu, Xuelong Zhang, Qiuyan Li, Xueyuan Jia, Jie Wu, Wenjing Sun, Yuandong Qiao, Jiawei Wu, Yuzhen Li, Jingcui Yu, Songbin Fu, Lidan Xu,