Abstract
BackgroundInterferon-beta (IFNβ) regulates the expression of a complex set of pro- as well as anti-inflammatory genes. In cohorts of MS patients unstratified for therapeutic response to IFNβ, normal vaccine-specific immune responses have been observed. Data capturing antigen-specific immune responses in cohorts of subjects defined by response to IFNβ-therapy are not available.ObjectiveTo assess antigen-specific immune responses in a cohort of MS patients responding clinically and radiologically to IFNβ.MethodsIn 26 MS patients, clinical and MRI disease activity were assessed before and under treatment with IFNβ. Humoral and cellular immune response to influenza vaccine was prospectively characterized in these individuals, and 33 healthy controls by influenza-specific Enzyme-Linked Immunosorbent Assay (ELISA) and Enzyme Linked Immuno Spot Technique (ELISPOT).ResultsRelated to pre-treatment disease activity, IFNβ reduced clinical and radiological MS disease-activity. Following influenza vaccination, frequencies of influenza-specific T cells and concentrations of anti-influenza A and B IgM and IgG increased comparably in MS-patients and in healthy controls.ConclusionsBy showing in a cohort of MS-patients responding to IFNβ vaccine-specific immune responses comparable to controls, this study indicates that antigen-specific immune responses can be preserved under successful IFNβ-therapy.
Highlights
Humoral and cellular immune response to influenza vaccine was prospectively characterized in these individuals, and 33 healthy controls by influenza-specific Enzyme-Linked Immunosorbent Assay (ELISA) and Enzyme Linked Immuno Spot Technique (ELISPOT)
By showing in a cohort of MS-patients responding to IFNb vaccine-specific immune responses comparable to controls, this study indicates that antigen-specific immune responses can be preserved under successful IFNb-therapy
IFNb, as all type I interferons (IFNa, IFNb, IFNe, IFNk, IFNx, and IFNv), binds to the IFNa receptor (IFNAR) [1], resulting in phosphorylation of signal transducer and activator of transcription (STAT) complexes that regulate the expression of a complex set of pro- as well as anti-inflammatory genes [2]
Summary
IFNb, as all type I interferons (IFNa, IFNb, IFNe, IFNk, IFNx, and IFNv), binds to the IFNa receptor (IFNAR) [1], resulting in phosphorylation of signal transducer and activator of transcription (STAT) complexes that regulate the expression of a complex set of pro- as well as anti-inflammatory genes [2]. Non-suppressed vaccine-induced inhibition of hemagglutination suggested some degree of selectivity of IFNb in suppressing autoimmune inflammation [11,12]. These studies were done in cohorts of patients that were not defined with regard to their response to IFNb-therapy. In search of a potential (subclinical) immuno-inhibitory effect of IFNb we here prospectively monitored humoral and cellular vaccine-specific immunity in a cohort of patients with MS defined by clinical and radiological response to IFNb-treatment as well as in healthy controls. Data capturing antigen-specific immune responses in cohorts of subjects defined by response to IFNb-therapy are not available
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