Pathogenesis of human systemic lupus erythematosus: recent advances.

Pathogenesis of human systemic lupus erythematosus: recent advances.
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DOI:
10.1016/j.molmed.2009.12.005
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发表时间:
2010-02
影响因子:
13.6
通讯作者:
Tsokos GC
Tsokos GC
中科院分区:
医学1区
文献类型:
--
作者:
Crispín JC;Liossis SN;Kis-Toth K;Lieberman LA;Kyttaris VC;Juang YT;Tsokos GC

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系统性红斑狼疮(SLE)是一种自身免疫性疾病,主要影响女性,表现为累及多个器官,包括肾脏、关节、神经系统和造血器官。免疫系统畸变以及遗传、激素和环境因素在器官损伤的表达中相互作用。最近来自不同领域的贡献,发展了我们对系统性红斑狼疮的理解和重塑目前的致病模型。在这里,我们回顾了新的信息,涉及1)与疾病表达相关的基因,2)导致自身免疫病理学的免疫细胞分子异常,3)激素和性染色体在疾病发展中的作用,4)环境和表观遗传因素被认为有助于SLE的表达。最后,我们强调与SLE疾病过程密切相关的分子缺陷,这些缺陷代表了理想的治疗靶点和疾病生物标志物。
Systemic lupus erythematosus (SLE) is an autoimmune disease that predominantly affects women and presents with manifestations derived from the involvement of multiple organs including the kidneys, joints, nervous system, and hematopoietic organs. Immune system aberrations, as well as heritable, hormonal, and environmental factors interplay in the expression of organ damage. Recent contributions from different fields have developed our understanding of SLE and reshaped current pathogenic models. Here, we review novel information that deals with 1) genes associated with disease expression, 2) immune cell molecular abnormalities that lead to autoimmune pathology, 3) the role of hormones and sex chromosomes in the development of disease, 4) environmental and epigenetic factors thought to contribute to the expression of SLE. Finally, we emphasize molecular defects intimately associated with the disease process of SLE that represent ideal therapeutic targets and disease biomarkers.
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影响因子: 27.4
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