Mahbubeh Rojhannezhad - PhD student of genetics department of genetics, Faculty of biological sciences, Tarbiat modares university
Abdorreza Naser Moghadasi - Tehran University of Medical Sciences, Department of Neurology
Abbas Nikravesh - Department of Medical Biotechnology & Molecular Sciences, Faculty of Medicine, Bojnord University
Mehrdad Behmanesh - Department of genetics, Faculty of biological sciences, Tarbiat modares university

Background and Objective: Multiple sclerosis (MS) is a chronic disease that involves an immune-mediated process in which an abnormal response of the body’s immune system is directed against the central nervous system (CNS). β-interferon (βIFN) is one of the first major therapies to control exacerbations in MS but it is only partially effective. Several Studies aim to identify molecular signature of βIFN clinical response in MS patients and also biomarkers that allow early identification of treatment failure or ideally even predict non-responder status. Materials and Methods: In this study we have reviewed several studies and analyzed microarray data (GSE5574) investigating gene expression patterns from longitudinal PBMC samples taken from patients prior to βIFN therapy and chronic post-treatment.Results and Conclusion: Analysis of the data showed that, not surprisingly genes related to pathways like interferon signaling, cytokine signaling and immune response are differentially expressed. Type I IFN-signalling pathway was the most significantly associated with the non-responder phenotype. Interferons (IFNs) are inducible cytokines with potent antiviral and anti-proliferative effects. In several autoimmune disorders such as rheumatoid arthritis, Sjögren s syndrome and also in a subgroup of MS patients (RRMS) IFN type I gene expression has been reported to be upregulated. Therefor it seems that common etiological factors and pathogenetic pathways operate in these autoimmune disorders. To validate this pathway as a prediction marker for βIFN clinical response further data analysis is needed.

multiple sclerosis, β-interferon , clinical response