AUTOANTIBODIES IN SYSTEMIC LUPUS ERYTHEMATOSUS: FROM PATHOGENIC MECHANISMS TO BIOMARKERS AND TARGETED THERAPEUTIC STRATEGIES

Abstract

Systemic Lupus Erythematosus (SLE) is a complex autoimmune condition marked by a breakdown in immune tolerance, leading to the production of autoantibodies against self-antigens. Disease progression is driven by these autoantibodies through immune complex formation, complement activation, and inflammatory responses, resulting in tissue damage and multi-organ involvement. Key autoantibodies including anti-dsDNA, anti-Sm, anti-Ro/SSA, anti-La/SSB, and anti-phospholipid antibodies not only contribute to disease pathogenesis but also serve as important biomarkers for diagnosis, prognosis, and monitoring disease activity. B-cell dysregulation, genetic susceptibility, epigenetic changes, and environmental factors have recently been recognized as key regulators of autoantibody production. While current therapies targeting immune cells and inflammatory pathways have improved SLE management, challenges such as disease heterogeneity, treatment resistance, and adverse effects persist. Advances in precision medicine, autoantibody profiling, and emerging therapies are opening new avenues for personalized care. This review summarizes the pathogenic mechanisms, clinical significance, and therapeutic potential of autoantibodies in SLE, with emphasis on their role in improving diagnosis and targeted treatment.