メラトニンは,多発性硬化症 の 再発 の 季節性 に 寄与 する
Mauricio F Farez1, Ivan D Mascanfroni2, Santiago P Méndez-Huergo3
1Center for Research on Neuroimmunological Diseases (CIEN), Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires 1428, Argentina.
Cell
|September 12, 2015
まとめ
メラトニンは夜間の長さに 影響するホルモンで 多発性硬化症 (MS) の活動を 減少させる可能性があります メラトニン治療は実験的なMSを改善し,T細胞の分化に影響を与え,この自己免疫疾患に対する潜在的な治療の洞察を提供します.
科学分野:
- 神経免疫学
- 内分泌学
- 自己免疫疾患
背景:
- 多発性硬化症 (MS) は 病気の活動に季節的な変化を示し 環境の影響を示唆しています
- メラトニンの生成は,光周期 (夜の長さ) の季節的変化によって制御される.
研究 の 目的:
- メラトニン濃度と多発性硬化症の活動との関連を調べる
- 実験的な自己免疫性脳髄炎 (EAE) のメラトニンの治療の可能性と,T細胞の分化に対する効果を調査する.
主な方法:
- 人間におけるメラトニン濃度とMSの相関分析
- MS (EAE) の実験モデルにおけるメラトニン治療
- ヒトとマウスのT細胞の分化に対するメラトニンのインビトロ分析,遺伝子発現 (Nfil3) とシグナル伝達経路 (Erk1/2,ROR-α) を含む.
主要な成果:
- ヒトのメラトニンのレベルは,MS疾患の活動と負の相関関係があります.
- メラトニン治療はEAEモデルで疾患の重症度を改善した.
- メラトニンは,Nfil3発現を誘導することで,病原性Th17細胞の分化を抑制した.
- メラトニンは,Erk1/ 2とROR-α媒介型IL-10プロモーターのトランスアクティベーションにより,保護性Tr1細胞生成を促進した.
結論:
- メラトニンはT細胞の分化に影響を与え,自己免疫疾患の病原性に影響を与えます.
- メラトニンのような環境要因は 多発性硬化症に関連する免疫反応を調節します
- メラトニンは,MSのような自己免疫疾患の管理のための潜在的な治療目標です.
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