Abstract
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease characterized by various types of immunological abnormalities including circulating and tissue-fixed autoantibodies reactive with autoantigens. The mechanism that can explain the production of these antibodies is unclear. Here we address the binding specificity of SLE autoantibodies with recombinant alpha interferon 2b (hrIFN alpha-2b), commercially available interferon (IFN alpha-2b), and the gene (cIFN alpha-2b) encoding this interferon. hrIFN alpha-2b showed higher binding with naturally occurring SLE autoantibodies as compared to IFN alpha-2b (p<0.05) or cIFN alpha-2b gene (p<0.001) as assessed by direct binding, inhibition ELISA, and quantitative precipitin titration. The relative affinity of SLE autoantibodies for hrIFN alpha-2b, IFN alpha-2b, and cIFN alpha-2b gene was in the order of 1.13x10(-7), 1.38x10(-6), and 1.22x10(-6), respectively. hrIFN alpha-2b is shown to have unique epitopes that would explain the possible antigenic role of hrIFN alpha-2b in the generation of SLE autoantibodies. Anti-hrIFN alpha-2b antibodies have been shown to represent an alternative immunological probe for the estimation of interferon alpha 2b in the serum of SLE patients.