Decoding the connection between SLE and DNA Sensors: A comprehensive review

Systemic lupus erythematosus (SLE) is recognized as a prevalent autoimmune disorder characterized by a multifaceted pathogenesis potentially influenced by a combination of environmental factors, genetic predisposition, and hormonal regulation. The continuous study of immune system activation is especially intriguing. Analysis of blood samples from individuals with SLE reveals an abnormal increase in interferon levels, along with the existence of anti-double-stranded DNA antibodies. This evidence suggests that the development of SLE may be initiated by innate immunity. The presence of abnormal dsDNA fragments can activate DNA sensors within cells, particularly immune cells, leading to the initiation of downstream signaling cascades that result in the upregulation of relevant cytokines and the subsequent initiation of adaptive immune responses, such as B cell differentiation and T cell activation. The intricate pathogenesis of SLE results in DNA sensors exhibiting a wide range of functions in innate immune responses that are subject to variation based on cell types, developmental processes, downstream effector signaling pathways and other factors. The review aims to reorganize how DNA sensors influence signaling pathways and contribute to the development of SLE according to current studies, with the aspiration of furnishing valuable insights for future investigations into the pathological mechanisms of SLE and potential treatment approaches.