Ye Fubiao, Lyu Feng-Juan, Wang Hua, Zheng Zhaomin
Department of Spine Surgery, The First Affiliated Hospital Sun Yat-Sen University Guangzhou China.
Department of Orthopaedics, Fujian Provincial Hospital Provincial Clinical Medical College of Fujian Medical University Fuzhou Fujian China.
JOR Spine. 2022 Mar 15;5(1):e1196. doi: 10.1002/jsp2.1196. eCollection 2022 Mar.
Intervertebral disc (IVD) herniation and degeneration contributes significantly to low back pain (LBP), of which the molecular pathogenesis is not fully understood. Disc herniation may cause LBP and radicular pain, but not all LBP patients have disc herniation. Degenerated discs could be the source of pain, but not all degenerated discs are symptomatic. We previously found that disc degeneration and herniation accompanied by inflammation. We further found that anti-inflammatory molecules blocked immune responses, alleviated IVD degeneration and pain. Based on our recent findings and the work of others, we hypothesize that immune system may play a prominent role in the production of disc herniation or disc degeneration associated pain. While the nucleus pulposus (NP) is an immune-privileged organ, the damage of the physical barrier between NP and systemic circulation, or the innervation and vascularization of the degenerated NP, on one hand exposes NP as a foreign antigen to immune system, and on the other hand presents compression on the nerve root or dorsal root ganglion (DRG), which both elicit immune responses induced by immune cells and their mediators. The inflammation can remain for a long time at remote distance, with various types of cytokines and immune cells involved in this pain-inducing process. In this review, we aim to revisit the autoimmunity of the NP, immune cell infiltration after break of physical barrier, the inflammatory activities in the DRG and the generation of pain. We also summarize the involvement of immune system, including immune cells and cytokines, in degenerated or herniated IVDs and affected DRG.
椎间盘（IVD）突出和退变是导致腰痛（LBP）的重要原因，其分子发病机制尚未完全明确。椎间盘突出可能导致腰痛和神经根性疼痛，但并非所有腰痛患者都有椎间盘突出。退变的椎间盘可能是疼痛的来源，但并非所有退变的椎间盘都有症状。我们之前发现椎间盘退变和突出伴有炎症。我们进一步发现抗炎分子可阻断免疫反应，减轻椎间盘退变和疼痛。基于我们最近的研究结果及其他研究成果，我们推测免疫系统可能在椎间盘突出或椎间盘退变相关疼痛的产生中起重要作用。虽然髓核（NP）是一个免疫豁免器官，但NP与体循环之间物理屏障的破坏，或退变NP的神经支配和血管化，一方面使NP作为外来抗原暴露于免疫系统，另一方面对神经根或背根神经节（DRG）造成压迫，这两者都会引发免疫细胞及其介质诱导的免疫反应。炎症可在远处长期存在，多种细胞因子和免疫细胞参与这一疼痛诱导过程。在本综述中，我们旨在重新审视NP的自身免疫性、物理屏障破坏后的免疫细胞浸润、DRG中的炎症活动以及疼痛的产生。我们还总结了免疫系统，包括免疫细胞和细胞因子，在退变或突出的IVD以及受影响DRG中的作用。
