Leveraging Type I Interferons: Exploring Pathogenesis and Therapeutic Strategies in Autoimmune Diseases

Type I interferons (IFN-I) exert a significant influence on the immune system. Produced by certain immune cells, they affect other immune cells and mediate diverse effects, including antiviral activity, inhibition of tumor growth, and suppression of cell proliferation. IFN-I is also implicated in the development and persistence of autoimmune disorders. Research has shown that abnormal IFN-I levels and IFN-I-regulated gene expression in the blood or tissues of individuals with autoimmune diseases are associated with disease onset, clinical manifestations, and severity. Monogenic conditions known as Type I interferonopathies-caused by mutations affecting the IFN-I signaling pathway-share clinical features with systemic lupus erythematosus (SLE). Both preclinical models and clinical trials targeting the IFN-I signaling pathway have yielded promising results for the treatment of autoimmune diseases. This review provides an overview of the interplay between epigenetics, various types of RNAs, transcription factors, and IFN-I. It discusses epigenetic modifications and transcription factor dysregulation, offering insights into disease mechanisms and potential future therapeutic advancements.