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首页> 外文会议>Annual Meeting of The American College of Veterinary Pathologists/American Society for Veterinary Clinical Pathology >Innate Immune Responses in Autoimmunity and the Pathogenesis of SLE
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Innate Immune Responses in Autoimmunity and the Pathogenesis of SLE

机译：自身免疫的先天免疫应答和SLE的发病机制

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Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease characterized by the production of autoantibodies and the involvement of various organ systems resulting in appreciable morbidity and mortality (1). These autoantibodies and immune complexes containing these autoantibodies accumulate in the joints, kidneys, and other tissues where they provoke inflammatory responses leading to tissue damage and destruction (2, 3). The etiology of SLE is poorly understood with disease resulting from a complex interaction between environmental and genetic factors leading to activation of both the innate and adaptive immune systems. The complexity and heterogeneity of human SLE is mirrored in animal models where a variety of genetic defects resulting in apoptotic pathway abnormalities, dysregulated B and T cell signaling cascades or impaired clearance of cell debris have been shown to result in a lupus-like phenotype (4, 5). Remarkably, in these different mouse models and in most SLE patients, the predominant autoantigens targeted are protein-nucleic acid macromolecules, either chromatin (protein-DNA macromolecules) or small nuclear ribonucleoproteins (protein-RNA macromolecules). Recent studies have indicated that these particular specificitiesmay be preferentially selected as a result of the ability of DNA and RNA autoantigens to induce immune responses through activation of Toll-like receptor 9 (TLR9) and TLR7 respectively.
机译：全身狼疮红斑（SLE）是一种炎症性自身免疫性疾病，其特征在于造成自身抗体和各种器官系统的累及，导致了明显的发病率和死亡率（1）。这些自身抗体和免疫复合物，含有这些自身抗体积聚在关节，肾脏和其他组织中，在那里他们挑选炎症反应导致组织损伤和破坏（2,3）。由于环境和遗传因素之间的复杂相互作用导致激活先天和适应性免疫系统，因此SLE的病因差异很差。人SLE的复杂性和异质性在动物模型中镜像，导致凋亡途径异常，呼吸困难的B和T细胞信号传导级联或细胞碎片的损伤的遗传缺陷已被证明导致狼疮样表型（4 5）。值得注意的是，在这些不同的小鼠模型和大多数SLE患者中，靶向的主要自身抗原是蛋白质 - 核酸大分子，染色质（蛋白质-DNA大分子）或小核核糖蛋白（蛋白质-RNA大分子）。最近的研究表明，由于DNA和RNA自身抗原能够分别激活Toll样受体9（TLR9）和TLR7，优先选择这些特定的特异性优先选择免疫应答。

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