Abstract
Aim of the study: Interferon alpha-induced arthritis and activation of the type 1 interferon pathway during rheumatoid arthritis (RA) has been well documented but the underlying mechanism remains unclear. This study addressed the binding specificity of antibodies with recombinant interferon alpha 2b (rIFN alpha-2b) in sera from different RA patients. Utilization of anti-hrIFN alpha-2b antibodies as a probe for estimation of interferon alpha-2b concentration in RA patients' synovial fluid (SF) was also investigated.
Material and methods: Binding specificities of antibodies from the sera of 60 RA patients and 35 controls subjects were studied by direct binding, inhibition ELISA, and quantitative precipitation titration. Inhibition ELISA was also used to estimate patients' SF interferon alpha-2b concentrations.
Results: RA IgG from patients' sera showed strong recognition to hrIFN alpha-2b in comparison to commercially available interferon (IFN alpha-2b) (p < 0.05) or the gene encoding this interferon (IFN alpha-2b gene) (p < 0.05). The affinity of RA antibodies for rIFN alpha-2b (1.10 x 10(-7) M) was found to be high as assessed by Langmuir plot. No significant difference in the level of interferon a in the SF of RA patients was observed as compared to the healthy controls.
Conclusions: rIFN alpha-2b presents unique epitopes that might explain the possible antigenic role in the induction of RA antibodies and anti-rIFN alpha-2b antibodies represent an alternative immunological probe for the estimation of interferon a in the SF of RA patients.