Department of Internal Medicine, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, Indonesia.
Department of Internal Medicine, Dr. Soetomo General Academic Hospital, Surabaya 60286, Indonesia.
Medicina (Kaunas). 2023 May 26;59(6):1033. doi: 10.3390/medicina59061033.
Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease that attacks various organ systems with a variety of clinical implications, ranging from mild skin and mucosal manifestations to severe central nervous system manifestations and death. Cases of SLE have been documented nearly two centuries ago when scholars used the terms 'erythema centrifugum' and 'seborrhea congestiva' to describe the discoid skin lesions and the butterfly or malar rash in SLE. Since then, knowledge about this disease has developed rapidly, especially knowledge related to the underlying pathogenesis of SLE. To date, it is known that immune system dysregulation, supported by genetic and environmental predisposition, can trigger the occurrence of SLE in a group of susceptible individuals. Various inflammatory mediators, cytokines and chemokines, as well as intra- and intercellular signaling pathways, are involved in the pathogenesis of SLE. In this review, we will discuss the molecular and cellular aspects of SLE pathogenesis, with a focus on how the immune system, genetics and the environment interact and trigger the various clinical manifestations of SLE.
系统性红斑狼疮（SLE）是一种全身性自身免疫性疾病，可攻击多种器官系统，具有多种临床意义，从轻到重依次为皮肤和黏膜表现、严重的中枢神经系统表现和死亡。近两个世纪前就有 SLE 的病例记录，当时学者们使用“离心性红斑”和“充血性脂溢性皮炎”来描述盘状皮肤损伤和蝶形或面颊皮疹。此后，人们对这种疾病的认识迅速发展，尤其是与 SLE 潜在发病机制相关的知识。迄今为止，人们已经知道，免疫系统失调在遗传和环境倾向的支持下，可能会在一组易感个体中引发 SLE。各种炎症介质、细胞因子和趋化因子以及细胞内和细胞间信号通路都参与了 SLE 的发病机制。在这篇综述中，我们将讨论 SLE 发病机制的分子和细胞方面，重点讨论免疫系统、遗传学和环境如何相互作用并引发 SLE 的各种临床表现。
