Wick Georg, Andersson Leif, Hala Karel, Gershwin M Eric, Selmi Carlo, Erf Gisela F, Lamont Susan J, Sgonc Roswitha
Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, A-6020 Innsbruck, Austria.
Adv Immunol. 2006;92:71-117. doi: 10.1016/S0065-2776(06)92002-1.
Autoimmune diseases in human patients only become clinically manifest when the disease process has developed to a stage where functional compensation by the afflicted organ or system is not possible anymore. In order to understand the initial etiologic and pathogenic events that are generally not yet accessible in humans, appropriate animal models are required. In this respect, spontaneously developing models--albeit rare--reflect the situation in humans much more closely than experimentally induced models, including knockout and transgenic mice. The present chapter describes three spontaneous chicken models for human autoimmune diseases, the Obese strain (OS) with a Hashimoto-like autoimmune thyroiditis, the University of California at Davis lines 200 and 206 (UCD-200 and -206) with a scleroderma-like disease, and the amelanotic Smyth line with a vitiligo-like syndrome (SLV). Special emphasis is given to the new opportunities to unravel the genetic basis of these diseases in view of the recently completed sequencing of the chicken genome.
人类自身免疫性疾病只有在疾病进程发展到患病器官或系统无法再进行功能代偿的阶段才会出现临床症状。为了了解通常在人类中尚无法知晓的初始病因和致病事件,需要合适的动物模型。在这方面,自发形成的模型——尽管罕见——比实验诱导模型(包括基因敲除和转基因小鼠)更能反映人类的情况。本章描述了三种人类自身免疫性疾病的自发鸡模型:患有桥本氏样自身免疫性甲状腺炎的肥胖品系(OS)、患有硬皮病样疾病的加利福尼亚大学戴维斯分校200系和206系(UCD - 200和 - 206),以及患有白癜风样综合征的无黑色素史密斯品系(SLV)。鉴于鸡基因组测序最近已完成,特别强调了利用这些新机会来揭示这些疾病的遗传基础。