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New genetic markers of psoriasis revealed

In the largest and most technologically advanced study of its kind, researchers have identified seven DNA "hotspots" that may reveal the role genetics plays in the development of psoriasis.

The study—conducted by Foundation supported scientists from the University of Michigan, University of Utah and Washington University in St. Louis, Mo.—revealed additional genetic components that contribute to the risks of developing psoriasis.

The researchers studied 1,359 psoriasis samples to determine which DNA changes, called single nucleotide polymorphisms (SNPs), were common among the samples. They then compared those common variations against at least 1,400 healthy samples (controls). After this first phase, they expanded the study to include 5,048 psoriasis samples and 5,051 controls to confirm psoriasis-related DNA changes.

"This fantastic new research brings us closer to understanding the complete genetic contribution to psoriasis," said Bruce Bebo Jr., director of research for the National Psoriasis Foundation. "In addition, these findings revealed a number of potential new psoriasis targets for treatments."

The seven common DNA variants, or SNPs, that have strong associations with psoriasis identified in the study are:


Interleukin-23A (IL23A), IL23R, IL12, IL4 and IL13—immune signaling molecules that control the strength and type of immune response


TNFAIP3 and TNIP1—genes that are activated by an immune signaling molecule called tumor necrosis factor-alpha (TNF-alpha), a known target for psoriasis modifying drugs.

Bebo said the Psoriasis Foundation contributed to the study by providing DNA samples from the Foundation's Tissue Bank, which was established in 1994 to house genetic material for psoriasis researchers.

The Foundation now collects genetic samples through the National Psoriasis Victor Henschel BioBank, created in 2006 to gather DNA to further study the genetics of psoriasis and increase understanding of the disease.

"There is still a long way to go to completely understand the contribution of genetics to psoriasis," Bebo said. "Donating your DNA to the BioBank—a sample of blood and a swab from your cheek—gives researchers access to the samples they need to complete this study and ultimately find a cure."

To donate DNA to the National Psoriasis BioBank, visit www.stoppsoriasis.org or call 800.723.9166, ext. 372 to learn more.

GOOGLE翻译

新闻和事件
新的遗传标记显示银屑病

在规模最大，技术最先进的同类研究，研究人员已经确定了七个DNA的“热点” ，可能揭示基因发挥作用的发展牛皮癣。

该研究进行了基金会支持科学家从密歇根大学，犹他大学和圣路易斯华盛顿大学，密苏里州，发现更多的遗传组成部分，有助于风险发展中国家牛皮癣。

研究人员研究了1359年银屑病样本，以确定哪些基因的变化，所谓的单核苷酸多态性（ SNPs ） ，是常见的样本。然后，他们相比，这些共同的变化至少在1400年健康的样本（控制） 。在第一阶段，他们扩大了研究，包括5048和5051型银屑病样品控制，以确认牛皮癣有关的基因变化。

“这美妙的新的研究使我们更接近于了解完整的遗传贡献牛皮癣，说： ”布鲁斯Bebo则称小的研究主管全国银屑病基金会。 “此外，这些研究结果揭示了一些潜在的新的治疗银屑病的目标。 ”

这七个共同的DNA变异，或单核苷酸多态性，即有强烈的协会银屑病研究中确定的是：


白细胞介素- 23A条（ IL23A ） ， IL23R ， IL12 ， IL4和IL13免疫信号分子控制的强度和类型的免疫应答


TNFAIP3和TNIP1 -基因被激活的免疫信号分子，叫做肿瘤坏死因子- α （ TNF - α ） ，一个已知的目标修改为银屑病药物。

Bebo则称银屑病基金会作出贡献的研究提供DNA样本基金会的组织银行，成立于1994年，房子为银屑病遗传物质的研究人员。

该基金会现在收集基因样本通过全国银屑病维克托亨舍尔生物库，创建于2006年收集的DNA进一步研究遗传学银屑病和提高认识的疾病。

“还有很长的路要走，才能完全理解的贡献遗传学牛皮癣， ” Bebo则称。 “捐赠您的DNA的生物库，血液样本和一个拭子从你的脸颊，使研究人员获得的样本，他们需要完成这项研究，并最终找到治愈。 ”

我只是提供外文资讯，简单地copy and paste. 翻译较花时间，毕竟楼上办了，谢谢。

张贴此文的目的是让各位比较前些时候所发表的合肥大学张教授的有关“易感基因”。到底是谁走在前面。有一点不同于外国的是：到底离开cure 有多远。张教授只字不提，让我们这些不大懂科学的是否今生今世有所期待。而NPF的文章里引用了Bebo 的话“还有很长的路要走，才能完全理解遗传学对银屑病的贡献。”这至少说明短期内１０～２０年不会有 cure.

今生可能等不到了。

彻底治愈，还有很长的路要走。

啥意思，能翻译一哈