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首页> 外文期刊>The Journal of dermatology >Current understanding of human genetics and genetic analysis of psoriasis
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Current understanding of human genetics and genetic analysis of psoriasis

机译：对人类遗传学和银屑病遗传分析的最新了解

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During the past 5 years, genome-wide association studies (GWAS), primarily based on single nucleotide polymorphism markers, have identified many loci as potential psoriasis susceptibility regions. These studies appeared to provide strong evidence because the susceptibility genes are involved in the interleukin-23/T-helper 17 axis of psoriasis immunopathogenesis and/or skin barrier functions. However, the "identified" genes only explained a small proportion of psoriasis heritability, although it is known to be comparatively higher than that of other common diseases. GWAS are based on the hypothesis that disease-causing variants are high frequency variants within populations. However, this hypothesis is problematic because deleterious variants such as those predisposing to specific diseases will generally not be maintained by selection pressure throughout human evolution. This issue also affects psoriasis studies. Here, we review the current paradigm shift in human genetic analyses and its implications for detection of psoriasis-causing variants based on linkage analysis and GWAS, except the well-known psoriasis susceptibility locus HLA-C.
机译：在过去的5年中，主要基于单核苷酸多态性标记的全基因组关联研究（GWAS）已确定许多位点为潜在的牛皮癣易感性区域。这些研究似乎提供了有力的证据，因为敏感性基因参与了牛皮癣免疫发病机制和/或皮肤屏障功能的白介素-23 / T-helper 17轴。然而，“已知”基因仅解释了牛皮癣遗传力的一小部分，尽管已知它比其他常见疾病要高。 GWAS基于以下假设：致病变异是人群中的高频变异。但是，这种假设是有问题的，因为有害的变异体（例如易患特定疾病的变异体）通常不会在整个人类进化过程中被选择压力所维持。此问题也影响牛皮癣研究。在这里，我们回顾了人类遗传学分析中的当前范式转移及其对基于连锁分析和GWAS的牛皮癣致病变异的检测的意义，除了著名的牛皮癣易感性基因座HLA-C。

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