| Title: | A pain-mediated neural signal induces relapse in murine autoimmune encephalomyelitis, a multiple sclerosis model |
| Authors: | Arima, Yasunobu Browse this author |
| Kamimura, Daisuke Browse this author →KAKEN DB |
| Atsumi, Toru Browse this author |
| Harada, Masaya Browse this author |
| Kawamoto, Tadafumi Browse this author →KAKEN DB |
| Nishikawa, Naoki Browse this author |
| Stofkova, Andrea Browse this author |
| Ohki, Takuto Browse this author |
| Higuchi, Kotaro Browse this author |
| Morimoto, Yuji Browse this author →KAKEN DB |
| Wieghofer, Peter Browse this author |
| Okada, Yuka Browse this author →KAKEN DB |
| Mori, Yuki Browse this author →KAKEN DB |
| Sakoda, Saburo Browse this author →KAKEN DB |
| Saika, Shizuya Browse this author →KAKEN DB |
| Yoshioka, Yoshichika Browse this author →KAKEN DB |
| Komuro, Issei Browse this author →KAKEN DB |
| Yamashita, Toshihide Browse this author →KAKEN DB |
| Hirano, Toshio Browse this author →KAKEN DB |
| Prinz, Marco Browse this author |
| Murakami, Masaaki Browse this author →KAKEN DB |
| Issue Date: | 11-Aug-2015 |
| Publisher: | eLife Sciences Publications |
| Journal Title: | eLife |
| Volume: | 4 |
| Start Page: | e08733 |
| Publisher DOI: | 10.7554/eLife.08733 |
| Abstract: | 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. |
| Rights: | http://creativecommons.org/licenses/by/4.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/61910 |
| Appears in Collections: | 遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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