HLA-C的着丝点区域是了解银屑病关节炎表型变异性的关键区域。

ISRN Dermatology Pub Date : 2014-01-30 eCollection Date: 2014-01-01 DOI:10.1155/2014/570178
Rubén Queiro, Patricia Tejón, Sara Alonso, Pablo Coto, Carlos López-Larrea, Jesús Martínez-Borra, Segundo González
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引用次数: 4

摘要

为了阐明HLA-C位点周围的几个多态性在PsA临床表达中的作用,我们分析了110例PsA患者、50例牛皮癣患者和110名健康对照者的HLA-C位点周围的几个多态性标记和基因的分布。这些基因的频率也通过PsA关节模型进行了分析,基于三个主要亚组:少关节炎、多关节炎和脊柱炎。远端指间关节(DIP)受累与MICB-CA20的存在相关(OR 6.0, 95% CI: 1.58-22.69, P = 0.005)。HLA-DRB∗07与PsA低关节形式相关(OR 4.1, 95% CI: 1.8-9.3, P = 0.0007)。脊柱体型过表达抗原HLA-B * 27 (OR 5.7, 95% CI: 2.4-13.6, P = 0.0001)。MICA-A5.1与多发性关节炎相关(OR 3.7, 95% CI: 1.5-8.8, P = 0.006)。HLA-C基因端粒在银屑病中过表达,而在PsA亚表型中无过表达。本研究表明,HLA-C的着丝点区域不仅是表达疾病风险基因的关键区域,也是表达有助于解释PsA表型变异性的基因的关键区域。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The Region Centromeric to HLA-C Is a Key Region for Understanding the Phenotypic Variability of Psoriatic Arthritis.

The Region Centromeric to HLA-C Is a Key Region for Understanding the Phenotypic Variability of Psoriatic Arthritis.

With the aim of clarifying the role of several polymorphisms around the HLA-C locus in the clinical expression of PsA, the distribution of several polymorphic markers and genes located around the HLA-C locus was analyzed in a well-established cohort of 110 patients with PsA, 50 patients with psoriasis alone, and 110 healthy controls. The frequency of these genes was also analyzed by PsA articular models, based on three main subgroups: oligoarthritis, polyarthritis, and spondylitis. Distal interphalangeal joint (DIP) involvement was associated with the presence of MICB-CA20 (OR 6.0, 95% CI: 1.58-22.69, P = 0.005). HLA-DRB∗07 was associated with oligoarticular forms of PsA (OR 4.1, 95% CI: 1.8-9.3, P = 0.0007). The spondylitic forms overexpressed the antigen HLA-B∗27 (OR 5.7, 95% CI: 2.4-13.6, P = 0.0001). MICA-A5.1 showed association with polyarthritis (OR 3.7, 95% CI: 1.5-8.8, P = 0.006). Genes telomeric to HLA-C were overexpressed in psoriasis but not in PsA subphenotypes. This study shows that the region centromeric to HLA-C is a key region that expresses not only disease risk genes but also genes that help explain the phenotypic variability of PsA.

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