在神经受伤后,自然杀手细胞退化完整的感官
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
概括
周围神经损伤会触发感官神经元中的早期视网酸1 (RAE1) 再表达,激活自然杀手 (NK) 细胞. 这导致受伤轴突的选择性退化,减少疼痛过敏.
科学领域:
- 神经科学
- 免疫学
- 细胞生物学
背景情况:
- 周围神经损伤可以保持轴突完整性尽管损伤.
- 感觉轴突在细胞体分离后退化, 但部分损伤呈现不同的情况.
- 对于治疗神经损伤至关重要.
研究的目的:
- 在外围神经受伤后感官轴突退化的过程中,研究酸早期1 (RAE1) 和自然杀伤细胞 (NK) 的作用.
- 探索选择性轴突清除背后的神经免疫机制.
- 评估调节NK细胞在神经性疼痛中的治疗潜力.
主要方法:
- 在受伤后的成年背根质神经元中对RAE1的再表达分析.
- 监测NK细胞透到坐骨神经.
- 使用遗传细胞切除和细胞因子-抗体复合刺激来研究NK细胞功能.
- 评估感官损失和受伤后的过敏.
主要成果:
- 在受伤的感觉神经元中重新表达RAE1,吸引细胞毒性NK细胞.
- 在压伤后3天内,NK细胞透到坐骨神经中.
- NK细胞的活性与受伤的附带体的退化和过敏性降低相关.
- 这种机制补充了瓦莱尔的退化.
结论:
- 一个涉及RAE1和NK细胞的新型神经免疫通路可以选择性地清除受损的感觉轴突.
- 通过清除部分受损的神经,调节NK细胞功能为疼痛神经病症提供了潜在的治疗策略.
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