Department of Biology, Drexel University, Philadelphia, PA, United States.
Institute of Cell Biology and Immunology, University Stuttgart, Stuttgart, Germany.
Front Immunol. 2021 Feb 22;12:641588. doi: 10.3389/fimmu.2021.641588. eCollection 2021.
Chronic neuropathic pain (CNP) is caused by a lesion or disease of the somatosensory nervous system. It affects ~8% of the general population and negatively impacts a person's level of functioning and quality of life. Its resistance to available pain therapies makes CNP a major unmet medical need. Immune cells have been shown to play a role for development, maintenance and recovery of CNP and therefore are attractive targets for novel pain therapies. In particular, in neuropathic mice and humans, microglia are activated in the dorsal horn and peripheral immune cells infiltrate the nervous system to promote chronic neuroinflammation and contribute to the initiation and progression of CNP. Importantly, immunity not only controls pain development and maintenance, but is also essential for pain resolution. In particular, regulatory T cells, a subpopulation of T lymphocytes with immune regulatory function, and macrophages were shown to be important contributors to pain recovery. In this review we summarize the interactions of the peripheral immune system with the nervous system and outline their contribution to the development and recovery of pain.
慢性神经性疼痛(CNP)是由躯体感觉神经系统的损伤或疾病引起的。它影响了约 8%的普通人群,并对人的功能水平和生活质量产生负面影响。其对现有疼痛疗法的抗性使得 CNP 成为一个主要的未满足的医疗需求。免疫细胞已被证明在 CNP 的发展、维持和恢复中发挥作用,因此是新型疼痛疗法的有吸引力的靶点。特别是在神经病理性小鼠和人类中,背角中的小胶质细胞被激活,外周免疫细胞浸润神经系统,以促进慢性神经炎症,并有助于 CNP 的起始和进展。重要的是,免疫不仅控制疼痛的发展和维持,而且对于疼痛的缓解也是必不可少的。特别是调节性 T 细胞(一种具有免疫调节功能的 T 淋巴细胞亚群)和巨噬细胞被证明是疼痛恢复的重要贡献者。在这篇综述中,我们总结了外周免疫系统与神经系统的相互作用,并概述了它们对疼痛发展和恢复的贡献。