神経損傷 の 後に 自然 の 殺人 細胞 は 無傷 の 感覚 器官 を 退化 さ せる
Alexander J Davies1, Hyoung Woo Kim2, Rafael Gonzalez-Cano3
1Dental Research Institute and Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul 03080, Republic of Korea; Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Cell
|February 5, 2019
まとめ
周回神経損傷は,感覚神経細胞におけるレチノ酸早期1 (RAE1) 再発現を誘発し,自然キラー (NK) 細胞を活性化させます. これは傷ついた軸索の選択的な変性につながり,痛みの過敏性を軽減します.
科学分野:
- 神経科学
- 免疫学
- 細胞生物学
背景:
- 辺縁神経の損傷は 損傷にもかかわらず軸索の整合性を保ちます
- 感覚軸索は細胞体の分離後に退化しますが 部分的な損傷は異なるシナリオを示します
- 神経損傷の治療には ウォレリアン変性以外のメカニズムを理解することが重要です
研究 の 目的:
- 外周神経損傷後の感覚軸索変性におけるレチノ酸早期1 (RAE1) と自然キラー (NK) 細胞の役割を調査する.
- 選択性軸索クリアランスの 神経免疫メカニズムを探る
- 神経疾患の痛みにおけるNK細胞の活性調節の治療の可能性を評価する.
主な方法:
- 大人の背根のギャングリアニューロンにおけるRAE1の再発分析
- 坐骨神経への NK 細胞の浸透を監視する
- 遺伝子細胞の除去と サイトカイン-抗体複合体の刺激を用いて NK細胞の機能を研究する.
- 感覚の喪失と怪我後の過敏性の評価
主要な成果:
- RAE1は損傷した感覚神経で再発し,細胞毒性NK細胞を惹きつけます.
- 麻痺傷害から3日以内にNK細胞が麻痺神経に浸透する.
- NK細胞の活動は,損傷したアファレントの退化と過敏性の低下と相関しています.
- このメカニズムは ヴァレリアンの退化を補完します
結論:
- RAE1とNK細胞を含む新しい神経免疫経路が 選択的に損傷した感覚軸索を浄化します
- 部分的に損傷した神経を浄化することで,痛ましい神経病に対する潜在的な治療戦略を提供します.
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