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Persistent exposure of the immune system to death cell debris leads to autoantibodies against chromatin in patients with systemic lupus erythematosus (SLE). Deposition of anti-chromatin/chromatin complexes can instigate inflammation in multiple organs including the kidney. Previously we identified specific cell death-associated histone modifications as targets of autoantibodies in SLE. In this study we addressed, in a large cohort of SLE patients and controls, the question whether plasma reactivities with specific histone peptides associated with serology and clinical features. Plasma from SLE patients with and without lupus nephritis, disease controls, and healthy controls, were tested in ELISA with histone H4 peptide acetylated at lysines 8, 12 and 16 (H4p ac ), H2B peptide acetylated at lysine 12 (H2Bp ac ), H3 peptide trimethylated at lysine 27 (H3p me ), and their unmodified equivalents. SLE patients displayed a higher reactivity with the modified equivalent of each peptide. Reactivity with H4p ac  showed both a high sensitivity (89%) and specificity (91%) for SLE, while H2Bp ac  exhibited a high specificity (96%) but lower sensitivity (69%). Reactivity with H3p me  appeared not specific for SLE. Anti-H4p ac  and anti-H2Bp ac  reactivity demonstrated a high correlation with disease activity. Moreover, patients reacting with multiple modified histone peptides exhibited higher SLEDAI and lower C3 levels. SLE patients with renal involvement showed higher reactivity with H2B/H2Bp ac  and a more pronounced reactivity with the modified equivalent of H3p me  and H2Bp ac . In conclusion, reactivity with H4p ac  and H2Bp ac  is specific for SLE patients and correlates with disease activity, whereas reactivity with H2Bp ac  is in particular associated with lupus nephritis.

Autoantibodies against Modified Histone Peptides in SLE Patients Are Associated with Disease Activity and Lupus Nephritis