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Correlation between anti‐interferon‐β binding and neutralizing antibodies in interferon‐β‐treated multiple sclerosis patients
Author(s) -
Jensen P. E. H.,
Sellebjerg F.,
Søndergaard H. B.,
Sørensen P. S.
Publication year - 2012
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2012.03721.x
Subject(s) - medicine , multiple sclerosis , interferon , antibody , immunology , virology
Background and purpose Measurements of binding antibodies ( BAb s), neutralizing antibodies ( NAb s) and MX1 mRNA expression are used to analyse the immunological reactions in patients with MS treated with IFN ‐β. The correlations between these are yet not fully understood. Methods We measured BAbs and NAb s to IFN ‐β in 110 serum samples from 83 patients with MS treated with IFN ‐β, and in a subgroup, antibody titre was compared with corresponding expressions of MX1 mRNA . The methods used were capture ELISA assay, luciferase reporter gene assay and mRNA RT ‐ PCR for MX1 gene expression. Results There were significant correlations between binding, neutralizing and MX1 results. Cut‐off values are suggested for the definition of samples of BAbs and NAb s as negative, positive and grey zones. Naturally occurring groups of low and high antibody titres were identified by the correlation between BAbs and NAb s, probably as a result of an immunological maturation process of antibodies. The low‐titre group had lower correlations between BAbs and NAb s than the high‐titre group. Conclusions High correlation is demonstrated between the results obtained by the three methods, and we suggest the possibility of using ELISA measurements of BAb s to identify patients with high titres of anti‐ IFN ‐β antibodies that block the biological response to IFN ‐β. Ιn patients with low titres, we suggest to supplement ELISA with measurement of MX1 mRNA to establish whether the bioavailability of IFN ‐β is preserved.