CLINICAL IMMUNOLOGY
Recombinant interferon alpha 2b in rheumatoid arthritis: good antigen for rheumatoid arthritis antibodies
Submission date: 2016-11-10
Final revision date: 2017-04-15
Acceptance date: 2017-04-18
Publication date: 2018-03-30
Cent Eur J Immunol 2018;43(1):58-68
KEYWORDS
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 α-2b) in sera from different RA patients. Utilization of anti-hrIFN α-2b antibodies as a probe for estimation of interferon α-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 α-2b concentrations.
Results:
RA IgG from patients’ sera showed strong recognition to hrIFN α-2b in comparison to commercially available interferon (IFN α-2b) (p < 0.05) or the gene encoding this interferon (IFN α-2b gene) (p < 0.05). The affinity of RA antibodies for rIFN α-2b (1.10 × 10–7 M) was found to be high as assessed by Langmuir plot. No significant difference in the level of interferon α in the SF of RA patients was observed as compared to the healthy controls.
Conclusions:
rIFN α-2b presents unique epitopes that might explain the possible antigenic role in the induction of RA antibodies and anti-rIFN α-2b antibodies represent an alternative immunological probe for the estimation of interferon α in the SF of RA patients.
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 α-2b) in sera from different RA patients. Utilization of anti-hrIFN α-2b antibodies as a probe for estimation of interferon α-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 α-2b concentrations.
Results:
RA IgG from patients’ sera showed strong recognition to hrIFN α-2b in comparison to commercially available interferon (IFN α-2b) (p < 0.05) or the gene encoding this interferon (IFN α-2b gene) (p < 0.05). The affinity of RA antibodies for rIFN α-2b (1.10 × 10–7 M) was found to be high as assessed by Langmuir plot. No significant difference in the level of interferon α in the SF of RA patients was observed as compared to the healthy controls.
Conclusions:
rIFN α-2b presents unique epitopes that might explain the possible antigenic role in the induction of RA antibodies and anti-rIFN α-2b antibodies represent an alternative immunological probe for the estimation of interferon α in the SF of RA patients.
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