Department of Neurology, The Second Hospital of Lanzhou University, Lanzhou, China.
Gansu Provincial Neurology Clinical Medical Research Center, The Second Hospital of Lanzhou University, Lanzhou, China.
Mol Brain. 2022 Aug 20;15(1):73. doi: 10.1186/s13041-022-00960-5.
Migraine is a complex neurological disease of unknown etiology involving both genetic and environmental factors. It has previously been reported that persistent pain may be mediated by the immune and inflammatory systems. Toll-like receptors (TLRs) play a significant role in immune and inflammatory responses and are expressed by microglia and astrocytes. One of the fundamental mechanisms of the innate immune system in coordinating inflammatory signal transduction is through TLRs, which protect the host organism by initiating inflammatory signaling cascades in response to tissue damage or stress. TLRs reside at the neuroimmune interface, and accumulating evidence has suggested that the inflammatory consequences of TLR activation on glia (mainly microglia and astrocytes), sensory neurons, and other cell types can influence nociceptive processing and lead to pain. Several studies have shown that TLRs may play a key role in neuropathic pain and migraine etiology by activating the microglia. The pathogenesis of migraine may involve a TLR-mediated crosstalk between neurons and immune cells. Innate responses in the central nervous system (CNS) occur during neuroinflammatory phenomena, including migraine. Antigens found in the environment play a crucial role in the inflammatory response, causing a broad range of diseases, including migraines. These can be recognized by several innate immune cells, including macrophages, microglia, and dendritic cells, and can be activated through TLR signaling. Given the prevalence of migraine and the insufficient efficacy and safety of current treatment options, a deeper understanding of TLRs is expected to provide novel therapies for managing chronic migraine. This review aimed to justify the view that TLRs may be involved in migraine.
偏头痛是一种病因不明的复杂神经系统疾病，涉及遗传和环境因素。先前有报道称，持续性疼痛可能由免疫和炎症系统介导。Toll 样受体 (TLR) 在免疫和炎症反应中起着重要作用，并由小胶质细胞和星形胶质细胞表达。固有免疫系统协调炎症信号转导的基本机制之一是通过 TLR，TLR 通过在组织损伤或应激时启动炎症信号级联反应来保护宿主生物。TLR 位于神经免疫界面，越来越多的证据表明，TLR 激活对神经胶质细胞（主要是小胶质细胞和星形胶质细胞）、感觉神经元和其他细胞类型的炎症后果会影响伤害性感受处理并导致疼痛。几项研究表明，TLR 通过激活小胶质细胞，在神经病理性疼痛和偏头痛发病机制中可能发挥关键作用。偏头痛的发病机制可能涉及神经元和免疫细胞之间的 TLR 介导的串扰。中枢神经系统 (CNS) 的固有反应发生在神经炎症现象中，包括偏头痛。环境中发现的抗原在炎症反应中起着至关重要的作用，导致包括偏头痛在内的多种疾病。几种固有免疫细胞（包括巨噬细胞、小胶质细胞和树突状细胞）可以识别这些抗原，并通过 TLR 信号激活它们。鉴于偏头痛的普遍性和当前治疗选择的疗效和安全性不足，预计对 TLR 的深入了解将为管理慢性偏头痛提供新的治疗方法。本综述旨在证明 TLR 可能与偏头痛有关。
