1 Immunopathogenesis of SLE

BSc, MSc Lesley J. Mason (Research Assistant), MD, FRCP David A. Isenberg (ARC Professor of Rheumatology)
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引用次数: 22

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease characterized by the deposition of autoantibodies and immune complexes, leading to tissue damage. The immunopathogenesis of SLE is like a jigsaw puzzle, some pieces of which are missing or have not fallen into place. In predisposed individuals, the initial stimulus is likely to be one or more of the environmental agents interacting with susceptibility genes.

Once the critical threshold is breached there is a failure of the immune system to downregulate the ensuing abnormal immune response, involving polyclonal B cell activation and hyperactive T cell help. Key questions include, what are the processes behind the availability of autoantigens and the breakdown of tolerance that give rise to the pathogenic autoantibodies? Current areas of research also involve the roles played by cytokines, adhesion molecules, co-stimulatory molecules and apoptosis.

1 SLE的免疫发病机制
系统性红斑狼疮(SLE)是一种自身免疫性风湿病,其特点是自身抗体和免疫复合物沉积,导致组织损伤。SLE的免疫发病机制就像一个拼图游戏,其中一些部分缺失或尚未到位。在易感个体中,最初的刺激可能是一种或多种与易感基因相互作用的环境因素。一旦突破临界阈值,免疫系统就无法下调随后的异常免疫反应,包括多克隆B细胞激活和过度活跃的T细胞帮助。关键问题包括,自身抗原的可用性和产生致病性自身抗体的耐受性分解背后的过程是什么?目前的研究领域还涉及细胞因子、粘附分子、共刺激分子和细胞凋亡的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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