Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a relapsing-remitting course, where periods of remission alternate with relapses of varying severity [1,2]. Exacerbations are a leading cause of irreversible organ damage accumulation, progression of disability, and reduced patient survival [4,6]. The article reviews current concepts regarding the pathogenesis of SLE relapses, including the role of innate and adaptive immune mechanisms, the interferon pathway, B-cell hyperactivation, and impaired immune complex clearance [3,4,12]. Particular attention is paid to clinical-immunological predictors of early relapse, including rising anti-dsDNA titers, hypocomplementemia, elevated BAFF and IL-6 levels, activation of the IFN-signature, and urinary biomarkers MCP-1 and TWEAK [1,16,20]. Data on multifactorial prediction models that allow forecasting exacerbations before clinical manifestation are summarized [4,12,7]. The presented review emphasizes the need to integrate laboratory, clinical, and molecular markers to create personalized algorithms for early detection and prevention of SLE relapses [11,13].

Systemic lupus erythematosus, relapse, pathogenesis

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