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. Author manuscript; available in PMC: 2012 Jul 18.
Published in final edited form as: Sci Transl Med. 2011 Mar 9;3(73):73ra19. doi: 10.1126/scitranslmed.3001180

Fig. 4.

Fig. 4

SLE patients develop autoantibodies against neutrophil antimicrobial peptides. (A) Antibodies to LL37, HNPs, and hBD in sera from patients with SLE (n = 38), scleroderma (n = 30), or healthy controls (HD; n = 12). Results are expressed as optical density (OD) index, which is the ratio of the OD in the patient serum to the mean OD in healthy control sera. Each symbol represents an independent patient, and horizontal bars represent the mean. *P = 0.002; **P < 0.0001; ***P = 0.023, ANOVA (adjusted for Dunnett’s test). n.s., not significant. (B) Percentages of SLE patients with or without significant anti-LL37 antibody titers (cutoff value OD index, 1.611; sensitivity, 41%; specificity, 100%; left panel) or SLE patients with or without anti-HNP antibody titers (cutoff value OD index, 1.15; sensitivity, 59%; specificity, 91%; right panel) among patients with detectable IFN-α (n = 9) and patients without IFN-α in the serum (n = 29). *P = 0.001; **P = 0.05, Fisher’s exact test. (C) IFN-α produced by pDC stimulation with in vitro–generated DNA-LL37/HNP complexes alone or with anti-LL37, anti-HNP, anti-DNA, or IgG control antibodies. One representative of at least three independent experiments is shown. Error bars represent the SD of triplicate wells.