Until recently, relapsing-remitting multiple sclerosis (RRMS) was considered a homogeneous form of multiple sclerosis (MS). Variability both in the immunopathology of active demyelinating lesions in MS and in response to immunomodulatory treatments has demonstrated that RRMS is a heterogeneous form of MS. An overwhelming number of trials have supported the use of interferon-β (IFN-β) as a first-line immunomodulatory treatment in RRMS. Approximately 30% of IFN-β treated RRMS patients are non-responders (NR) to treatment. Despite vast clinical experience in the use of IFN-β, its mechanisms of action have not been fully clarified. Interleukin-17 (IL-17) is a proinflammatory cytokine that is secreted by a lineage of T cells named Th17 cells. The Th17 chemokine pathways are essential for the development of central nervous system (CNS) autoimmune diseases such as MS. A high IL-17 concentration in the serum. of people with RRMS is associated with nonresponse to IFN-β therapy. Some animal and human studies have shown that IFN-β inhibits the activity of Th17 cells.
