Document Type: Special Articles

Authors

1 MSc Student, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran.

2 Assistant Professor, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran

3 MSc Student, Department of Biology, School of Sciences, University of Isfahan, Isfahan, Iran

Abstract

Multiple sclerosis (MS) is one of the most important autoimmune diseases recognized by demyelination and axonal lesion. It is the most common cause of disability in the young population. Various immunomodulatory and immunosuppressive therapies, including different formulations of interferon beta (IFNβ), glatiramer acetate (GA), mitoxantrone, and natalizumab are available for this disease. However, interferon has been the best prescribed. Although the precise mechanism of IFNβ is unclear, many studies indicate some potential mechanism including blocking T cells activation, controlling pro- and anti-inflammatory cytokine secretion, preventing activated immune cell migration through BBB, and inducing repair activity of damaged nerve cells by differentiating neural stem cells into oligodendrocytes. These molecular mechanisms have significant roles in IFNβ therapy. More researches are required in order for us to comprehend the mechanism of action of IFNβ, and improve and develop drugs for more efficient MS treatment.