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A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model
Yasunobu Arima (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Daisuke Kamimura (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Toru Atsumi (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Masaya Harada (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Tadafumi Kawamoto (Tsurumi University), Naoki Nishikawa (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Andrea Štofková (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Takuto Ohki (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Kotaro Higuchi (Hokkaido University, Institute for Genetic Medicine, Hokkaido University), Yuji Morimoto (Hokkaido University), Peter Wieghofer (University of Freiburg), Yuka Okada (Wakayama Medical University), Yuki Mori (Immunology Frontier Research Center, The University of Osaka, The University of Osaka), Saburo Sakoda (Toneyama National Hospital, National Hospital Organization), Shizuya Saika (Wakayama Medical University), Yoshichika Yoshioka (Immunology Frontier Research Center, The University of Osaka, The University of Osaka), Issei Komuro (The University of Tokyo), Toshihide Yamashita (The University of Osaka), Toshio Hirano (The University of Osaka), Marco Prinz (University of Freiburg), Masaaki Murakami (Hokkaido University, Institute for Genetic Medicine, Hokkaido University)
Résumé : Although pain is a common symptom of various diseases and disorders, its contribution to disease pathogenesis is not well understood. Here we show using murine experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS), that pain induces EAE relapse. Mechanistic analysis showed that pain induction activates a sensory-sympathetic signal followed by a chemokine-mediated accumulation of MHC class II+CD11b+ cells that showed antigen-presentation activity at specific ventral vessels in the fifth lumbar cord of EAE-recovered mice. Following this accumulation, various immune cells including pathogenic CD4+ T cells recruited in the spinal cord in a manner dependent on a local chemokine inducer in endothelial cells, resulting in EAE relapse. Our results demonstrate that a pain-mediated neural signal can be transformed into an inflammation reaction at specific vessels to induce disease relapse, thus making this signal a potential therapeutic target.