Wang Xiaocui, Wen Bin, Duan Xuemei, Zhang Yunfei, Hu Ying, Li Haonan, Shang Huifeng, Jing Yukai
Department of Clinical Laboratory, Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, 030032, People's Republic of China.
Department of Clinical Laboratory, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 030032, People's Republic of China.
J Inflamm Res. 2025 Mar 30;18:4533-4549. doi: 10.2147/JIR.S516195. eCollection 2025.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with multiple organ damage. Several studies have found that, in addition to significant production of autoantibodies, the majority of SLE patients exhibit increased expression of type I interferon (IFN-I) regulated genes (also known as IFN-I traits), and that IFN-I plays a crucial role in the pathogenesis of SLE. In SLE, virtually all immune cells are dysregulated, and most of these aberrant dysregulations are directly or indirectly affected by IFN-I. The mechanism of action of IFN-I in these immune cells is multifaceted. In this review, we focus on the immune cell types that produce IFN-I and are affected by IFN-I in SLE. Importantly, we explore the research progress of related drugs in terms of IFN-I production, itself, and downstream. Here we provide the most up-to-date information on the mechanisms that lead to the pathogenesis of SLE, providing the basis for the development of innovative future therapies and future research directions.
系统性红斑狼疮（SLE）是一种可导致多器官损害的慢性自身免疫性疾病。多项研究发现，除了大量产生自身抗体外，大多数SLE患者还表现出I型干扰素（IFN-I）调控基因的表达增加（也称为IFN-I特征），且IFN-I在SLE的发病机制中起关键作用。在SLE中，几乎所有免疫细胞都存在失调，其中大多数异常失调直接或间接受到IFN-I的影响。IFN-I在这些免疫细胞中的作用机制是多方面的。在本综述中，我们重点关注在SLE中产生IFN-I并受IFN-I影响的免疫细胞类型。重要的是，我们从IFN-I的产生、IFN-I本身以及其下游等方面探讨相关药物的研究进展。在此，我们提供了关于导致SLE发病机制的最新信息，为未来创新疗法的开发和未来研究方向提供依据。
