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Interferon β (IFNβ) is an approved immunomodulatory treatment of multiple sclerosis (MS). However, treatment with type I interferons may induce autoimmune diseases.1 This has mainly been shown for interferon α, but is not uncommon for IFNβ. Published results on humoral organ autoimmunity in IFNβ-treated patients with MS are not unequivocal at present.2,3
We therefore measured autoantibodies (AAbs) against major thyroid (thyroperoxidase [TPO] and thyroglobulin [Tg]) and pancreatic β-cell (glutamic acid decarboxylase [GAD65]) autoantigens in a large cohort of patients with MS treated with IFNβ or IFNβ treatment naïve. In the former, the presence of IFNβ neutralizing antibody (NABs) was correlated to AAbs seropositivity, as NABs may be an indicator of an activated humoral immune response.
Methods.
AAbs were determined by commercial radioligand assays against GAD65 (Medipan, Leipzig, Germany) and against TPO and Tg (BRAHMS, Hennigsdorf, Germany) with predefined cutoff levels (table) in 209 IFNβ-treated patients with MS and an age- and sex-matched control group of 57 IFNβ-naïve patients with MS. In the treated patients, presence of NABs was assessed by capture ELISA and ex vivo MxA real time rtPCR 12 hours after administration of IFNβ as described previously.4 Briefly, detection of binding antibodies by ELISA and demonstration of inhibition of MxA mRNA induction in peripheral blood lymphocytes at least once deemed a sample NAB positive. Statistical tests were performed using GraphPad Prism 4.0.
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Table Demographics (upper part) and autoantibody results (lower part) in …
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