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首页> 外文期刊>International journal of immunogenetics >Understanding the genetics of autoimmune disease: two loci that regulate late onset Addison's disease in Portuguese Water Dogs.
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Understanding the genetics of autoimmune disease: two loci that regulate late onset Addison's disease in Portuguese Water Dogs.

机译：了解自身免疫性疾病的遗传学：调节葡萄牙水犬中迟发性艾迪生氏病的两个基因座。

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Addison's disease, an immune-mediated disorder caused by destruction of the adrenal glands, is a rare disorder of Western European populations. Studies indicate that the disorder is polygenic in nature, involving specific alleles of the CTLA-4, DRB1*04 and DQ, Cyp27B1, VDR and MIC-A and -B loci. A similar immune form of Addison's disease occurs in several breeds of domestic dog, with frequencies ranging from 1.5 to 9.0%. The high frequency of the disease in domestic dog breeds likely reflects the small number of founders associated with many breeds, subsequent inbreeding, and the frequent use of popular sires. The Portuguese Water Dog (PWD) is a significantly affected breed. An analysis of 11,384 PWDs surveyed between 1985 and 1996 suggests a breed-specific disease incidence of 1.5%. As with humans, the disease is typically of late onset. This study involves a genetic comparison of Addison's disease in the PWD to the analogous disease in humans. The study is facilitated by the existence of complete pedigrees and a relatively high degree of inbreeding among PWDs. The breed originated from 31 founders, with 10 animals responsible for 90% of the current gene pool. We describe, specifically, the identification of two disease-associated loci, on Canis familiaris (CFA) chromosomes CFA12 and 37, which are syntenic with the human DRB1 histocompatibility locus alleles HLA-DRB1*04 and DRB1*0301, and to a locus for immunosuppression syntenic with CTLA-4. Strong similarities exist therefore in the complex genetic background of Addison's disease in humans and in the PWD. With the completion of the canine and human genome sequence, the purebred dog is set to become an important comparative model for Addison's as well as other human immune disorders.
机译：艾迪生氏病是一种由肾上腺破坏引起的免疫介导的疾病，是西欧人群中罕见的疾病。研究表明该疾病本质上是多基因的，涉及CTLA-4，DRB1 * 04和DQ，Cyp27B1，VDR和MIC-A和-B基因座的特定等位基因。类似的艾迪生氏病免疫形式发生在几种家犬中，频率范围为1.5％至9.0％。家犬品种中这种疾病的高发率很可能反映了与许多品种相关的创始人少，随后的近交和流行公犬的频繁使用。葡萄牙水犬（PWD）是一个受到严重影响的犬种。对1985年至1996年间调查的11,384名PWD的分析表明，特定疾病的发病率为1.5％。与人类一样，该疾病通常是晚期发作。这项研究涉及PWD中Addison病与人类类似疾病的遗传比较。完整谱系的存在和残疾人的近亲繁殖程度相对较高，从而促进了这项研究。该品种起源于31位创始人，其中10只动物占当前基因库的90％。我们具体描述了两个与疾病相关的基因座的识别，位于犬种（CFA）染色体CFA12和37上，与人类DRB1组织相容性基因座等位基因HLA-DRB1 * 04和DRB1 * 0301同系，与CTLA-4的免疫抑制同义。因此，人类和PWD中复杂的艾迪生氏病遗传背景存在着很强的相似性。随着犬和人类基因组序列的完成，纯种狗将成为艾迪生氏症以及其他人类免疫疾病的重要比较模型。

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