Comparison of the Expression of Mir-326 Between Interferon Beta Responders and Non-Responders in Relapsing-Remitting Multiple Sclerosis

Objective: multiple sclerosis (ms) is an inflammatory disease resulting in demyelination of the central nervous system (cns). t helper 17 (th17) subset protects the human body against pathogens and induces neuroinflammation, which leads to neurodegeneration. micrornas (mirnas) are a specific class of small (~22 nt) non-coding rnas that act as post-transcriptional regulators. the expression of the mir-326 is highly associated with the pathogenesis of ms disease in patients through the promotion of th17 development. recently, studies showed that disease-modifying therapies (dmts) could balance the dysregulation of mirnas in the immune cells of patients with relapsing-remitting ms (rrms). interferon-beta (ifn-β) has emerged as one of the most common drugs for the treatment of rr-ms patients. the purpose of this study was to evaluate the expression of the mir-326 in rrms patients who were responders and nonresponders to ifn-β treatment. materials and methods: in this cross-sectional study, a total of 70 patients (35 responders and 35 non-responders) were enrolled. we analyzed the expression of the mir-326 in peripheral blood mononuclear cells (pbmcs) of rrms patients at least one year after the initiation of ifn-β therapy. real-time polymerase chain reaction (rt-pcr) was applied to measure the expression of the mir-326. results: the results showed no substantial change in the expression of the mir-326 between responders and nonresponders concerning the treatment with ifn-β. although the expression of the mir-326 was slightly reduced in ifn-β-responders compared with ifn-β-non-responders; however, the reduction of the mir-326 was not statistically significant. conclusion: overall, since ifn-β doesn’t normalize abnormal expression of mir-326, this might suggest that ifn-β affects th17 development through epigenetic mechanisms other than mir-326 regulation.