系统性红斑狼疮的发病机制和潜在的治疗靶点:从实验到临床。

Q1 Medicine
Auto-Immunity Highlights Pub Date : 2014-08-14 eCollection Date: 2014-09-01 DOI:10.1007/s13317-014-0058-y
D Squatrito, G Emmi, E Silvestri, L Ciucciarelli, M M D'Elios, D Prisco, L Emmi
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引用次数: 39

摘要

系统性红斑狼疮(SLE)被认为是一种多器官受累的自身免疫性疾病。在过去十年中,关于炎症途径、遗传和表观遗传改变、适应性和先天免疫系统机制特异性参与SLE发病机制的研究取得了许多进展。早在十多年前,细胞凋亡就被认为是SLE发病机制中的一个重要角色。然而,直到最近,新的关键凋亡途径才被研究,并且含有自身抗原的凋亡碎片、先天免疫和持续炎症之间的联系已被进一步阐明。更好地了解细胞机制和相关细胞因子有助于开发专门针对SLE治疗的新生物药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside.

Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside.

Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside.

Pathogenesis and potential therapeutic targets in systemic lupus erythematosus: from bench to bedside.

Systemic lupus erythematosus (SLE) is considered an autoimmune disease with multiorgan involvement. Many advances have been made during the last decade regarding inflammatory pathways, genetic and epigenetic alterations, adaptive and innate immune system mechanisms specifically involved in SLE pathogenesis. Apoptosis has been proposed as an important player in SLE pathogenesis more than a decade ago. However, only recently new key apoptotic pathways have been investigated and the link between apoptotic debris containing autoantigens, innate immunity and ongoing inflammation has been further elucidated. Better understanding of cellular mechanisms and involved cytokines contributed to the development of new biological drugs specifically addressed for SLE therapy.

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