This is the authors' abstract. We don't add key points for this paper.
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.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: