INTRODUCTION
Multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) are demyelinating inflammatory diseases of the central nervous system (CNS) [1,2]. Many previous studies have revealed the important roles of inflammatory mediators, including cytokines, in the pathogenesis of MS and NMOSD [3-8]. Substances derived from damaged autologous tissues, called damage-associated molecular patterns (DAMPs), are attracting attention in the field of autoimmune diseases because they function as inflammatory mediators when released from cells [9,10]. We previously reported increased levels of high mobility group box 1 (HMGB1), a DAMP, in the serum of MS patients and the cerebrospinal fluid (CSF) from MS and NMOSD [4]. We also reported a significant positive correlation between CSF HMGB1 levels and CSF cells in patients with MS and NMOSD [4]. These findings indicate that HMGB1 may be involved with inflammation in MS and NMOSD. Also, the administration of anti-HMGB1 monoclonal antibodies ameliorated clinical symptoms, CNS inflammation, demyelination, and serum IL-17 upregulation in experimental autoimmune encephalomyelitis (EAE) [11]. These findings suggest that HMGB1 may control autoimmune responses by stimulating the release of inflammatory cytokines in MS. Recently, peroxiredoxins (PRXs), which are intracellular antioxidant enzymes, attract attention as novel DAMPs. Extracellular PRXs also induce the production of inflammatory cytokines and triggers inflammation; the pro-inflammatory effects of PRXs are reported to be stronger than that of HMGB1 [12]. Besides increasing inflammation, PRXs was reported to affect the blood–brain barrier function [13], which is another important factor in the pathogenesis of MS and NMOSD [14]. We speculate that PRXs could be key players in the inflammatory response of demyelinating CNS disorders, including MS and NMOSD, and could be a future therapeutic target. However, the exact function of PRXs in the pathogenesis of MS and NMOSD is not yet fully understood. The main aim of this study is to determine whether PRXs are involved in promoting inflammatory processes and affecting the blood–brain barrier function in patients with MS and NMOSD.