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Key Points Oxidative stressgenerated through multiple mechanisms in a cell-type-specific manneris a substantial contributor to disease pathogenesis, organ damage and comorbidities in patients with systemic lupus erythematosus (SLE) Pathways of oxidative pathogenesis, such as oxidative modification of self antigens and T-cell dysfunction, have been identified Organ systems in which the clinical importance of oxidative damage in SLE has been recognized include the cardiovascular and renal systems and the skin Biomarkers of oxidative stress correlate directly with disease activity in SLE Depletion of glutathione (reflecting oxidative stress) might have a pathogenic role

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This modification renders the peptide resistant to enzymatic degradation, significantly extending its half-life and potency in vivo compared to standard L-peptides

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