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Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective
Trends in Molecular Medicine ( IF 13.6 ) Pub Date : 2017-06-13 , DOI: 10.1016/j.molmed.2017.05.006
Vaishali R. Moulton , Abel Suarez-Fueyo , Esra Meidan , Hao Li , Masayuki Mizui , George C. Tsokos

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease affecting multiple organs. A complex interaction of genetics, environment, and hormones leads to immune dysregulation and breakdown of tolerance to self-antigens, resulting in autoantibody production, inflammation, and destruction of end-organs. Emerging evidence on the role of these factors has increased our knowledge of this complex disease, guiding therapeutic strategies and identifying putative biomarkers. Recent findings include the characterization of genetic/epigenetic factors linked to SLE, as well as cellular effectors. Novel observations have provided an improved understanding of the contribution of tissue-specific factors and associated damage, T and B lymphocytes, as well as innate immune cell subsets and their corresponding abnormalities. The intricate web of involved factors and pathways dictates the adoption of tailored therapeutic approaches to conquer this disease.



中文翻译:

人类系统性红斑狼疮的发病机制:细胞的角度。

系统性红斑狼疮(SLE)是一种慢性自身免疫性疾病,会影响多个器官。遗传,环境和激素的复杂相互作用导致免疫失调和对自身抗原的耐受性破坏,从而导致自身抗体的产生,炎症和终末器官的破坏。这些因素作用的新证据增加了我们对这种复杂疾病的认识,指导了治疗策略并确定了可能的生物标志物。最近的发现包括与SLE相关的遗传/表观遗传因素以及细胞效应子的表征。新颖的观察结果提供了对组织特异性因子和相关损伤,T和B淋巴细胞以及先天免疫细胞亚群及其相应异常的贡献的更好理解。

更新日期:2017-06-13
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