Recent Advances of Type I Interferon on the Regulation of Immune Cells and the Treatment of Systemic Lupus Erythematosus

Xiaocui Wang,1,* Bin Wen,2,* Xuemei Duan,1 Yunfei Zhang,1 Ying Hu,1 Haonan Li,1 Huifeng Shang,2 Yukai Jing1 1Department 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; 2Department 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*These authors contributed equally to this workCorrespondence: Yukai Jing, 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, Tel +86-13834234594, Email [email protected] Huifeng Shang, Department of Clinical Laboratory, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Tongji Shanxi Hospital, Taiyuan, 030032, People’s Republic of China, Email [email protected]: 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.Keywords: systemic lupus erythematosus, type I interferon, autoimmune, B cell, T cell