TY - JOUR T1 - Interleukin-19 alleviates experimental autoimmune encephalomyelitis by attenuating antigen-presenting cell activation JF - bioRxiv DO - 10.1101/2020.07.15.204826 SP - 2020.07.15.204826 AU - Hiroshi Horiuchi AU - Bijay Parajuli AU - Hiroyasu Komiya AU - Yuki Ogawa AU - Shijie Jin AU - Keita Takahashi AU - Yasu-Taka Azuma AU - Fumiaki Tanaka AU - Akio Suzumura AU - Hideyuki Takeuchi Y1 - 2020/01/01 UR - http://biorxiv.org/content/early/2020/07/17/2020.07.15.204826.abstract N2 - Interleukin-19 (IL-19) acts as an anti-inflammatory cytokine in various inflammatory diseases. Multiple sclerosis (MS) is a major neuroinflammatory disease in the central nervous system, but it remains uncertain how IL-19 contributes to MS pathogenesis. Here, we demonstrate that IL-19 deficiency aggravates experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by promoting IL-17–producing helper T cell (Th17 cell) infiltration into the central nervous system. In addition, IL-19–deficient splenic macrophages expressed elevated levels of major histocompatibility complex class II, co-stimulatory molecules, and Th17 cell differentiation–associated cytokines such as IL-1β, IL-6, IL-23, TGF-β1, and TNF-α. These observations indicated that IL-19 plays a critical role in suppression of MS pathogenesis by inhibiting macrophage antigen presentation, Th17 cell expansion, and subsequent inflammatory responses. Furthermore, treatment with IL-19 significantly abrogated EAE. Our data suggest that IL-19 could provide significant therapeutic benefits in patients with MS.Competing Interest StatementThe authors have declared no competing interest. ER -