Noninvasive diagnosis of ruptured peripheral atherosclerotic lesions and myocardial infarction by antibody profiling
J. Clin. Invest. Kitty B.J.M. Cleutjens, et al. 118:2979 doi:10.1172/JCI32767 [Go to this article.]

Figure 3
Specificity of the E1 and E12 autoantibody signature. (A and B) Ability of synthetic peptides E1 and E12 to deplete human ruptured sera from autoantibodies directed against phage E1 (A) and E12 (B), respectively. Data are mean ± SD. (C) Serum IgG content in patients with peripheral vascular disease. (D) Serum reactivity of 23 age- and sex-matched RA sera against clones E1 and E12. Filled symbols represent nonreactive sera; open symbols represent reactive sera. (E and F) Temporal pattern of the antibody profile to clones E1 (E) and E12 (F) in 10 patients with AMI. (G) Serum reactivity of 11 patients with non–atherosclerosis-related cardiac diagnoses. (A, B, and D–G) Reactivity is represented as the ratio of OD₄₅₀ sample/(mean OD₄₅₀ + 3SD) for empty phage. (C, D, and G) Data points and horizontal bars represent reactivity of individual sera and mean reactivity, respectively. *P < 0.05 versus nondepleted.