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A genetic basis for shared autoimmunity in mouse models.

机译:小鼠模型中共有自身免疫的遗传基础。

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Development of autoimmune disease is the result of activation of the immune system that subsequently leads to tissue destruction. Although the clinical outcome significantly differs between autoimmune diseases, some pathogenic pathways could be shared. During the recent years, intense efforts to find the genetic factors behind development of the complex and polygenic autoimmune diseases have been undertaken. The difficulties in addressing what genetic factors predispose for autoimmunity in humans underline the importance of animal models in the understanding of the general mechanisms behind the initiation of disease. Interestingly, it has been observed in studies of experimental models of autoimmune diseases, that many of the genetic linkages to disease development are located in the same genetic regions and potentially could be controlled by the same gene. Furthermore, comparison of the mouse/rat genetic regions with regions of association to human inflammatory diseases, also demonstrates some homologous loci between species. Some mouse strains can develop disease in more than one model for autoimmunity. This not only argues for some general mechanisms, but it also supports mechanisms related to the specific tissues attacked in the various autoimmune diseases. Here, we will discuss some aspects of shared autoimmunity in mouse models from a genetic point of view.
机译:自身免疫性疾病的发展是免疫系统激活的结果,其随后导致组织破坏。尽管自身免疫疾病之间的临床结局显着不同,但可以共享某些致病途径。近年来,人们为寻找复杂和多基因自身免疫性疾病发展的遗传因素付出了巨大的努力。解决人类自身免疫易感性的遗传因素的困难突显了动物模型在理解疾病引发的一般机制中的重要性。有趣的是,在自身免疫性疾病实验模型的研究中已经观察到,与疾病发展有关的许多遗传联系都位于相同的遗传区域,并且可能由相同的基因控制。此外,将小鼠/大鼠的遗传区域与与人类炎症性疾病相关的区域进行比较,还表明了物种之间的某些同源基因座。一些小鼠品系可以在一种以上的自身免疫模型中发展疾病。这不仅证明了一些通用的机制,而且还支持了与各种自身免疫疾病中攻击的特定组织有关的机制。在这里,我们将从遗传学角度讨论小鼠模型中共有自身免疫的某些方面。

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