IRCCS Istituto Ortopedico Galeazzi, 20161 Milan, Italy.
School of Medicine, Università Vita-Salute San Raffaele, 20132 Milan, Italy.
Int J Mol Sci. 2020 Feb 11;21(4):1186. doi: 10.3390/ijms21041186.
Fibromyalgia is one of the most important "rheumatic" disorders, after osteoarthritis. The etiology of the disease is still not clear. At the moment, the most defined pathological mechanism is the alteration of central pain pathways, and emotional conditions can trigger or worsen symptoms. Increasing evidence supports the role of mast cells in maintaining pain conditions such as musculoskeletal pain and central sensitization. Importantly, mast cells can mediate microglia activation through the production of proinflammatory cytokines such as IL-1β, IL-6, and TNFα. In addition, levels of chemokines and proinflammatory cytokines are enhanced in serum and could contribute to inflammation at systemic level. Despite the well-characterized relationship between the nervous system and inflammation, the mechanism that links the different pathological features of fibromyalgia, including stress-related manifestations, central sensitization, and dysregulation of the innate and adaptive immune responses is largely unknown. This review aims to provide an overview of the current understanding of the role of adaptive immune cells, in particular T cells, in the physiopathology of fibromyalgia. It also aims at linking the latest advances emerging from basic science to envisage new perspectives to explain the role of T cells in interconnecting the psychological, neurological, and inflammatory symptoms of fibromyalgia.
纤维肌痛是继骨关节炎之后最重要的“风湿性”疾病之一。该疾病的病因仍不清楚。目前，最明确的病理机制是中枢疼痛途径的改变，情绪状况可以引发或加重症状。越来越多的证据支持肥大细胞在维持肌肉骨骼疼痛和中枢敏化等疼痛状况中的作用。重要的是，肥大细胞可以通过产生白细胞介素-1β、白细胞介素-6 和肿瘤坏死因子-α 等促炎细胞因子来介导小胶质细胞的激活。此外，趋化因子和促炎细胞因子的水平在血清中增强，并可能导致全身炎症。尽管神经系统和炎症之间的关系已经得到很好的描述，但将纤维肌痛的不同病理特征（包括与压力相关的表现、中枢敏化和先天及适应性免疫反应失调）联系起来的机制在很大程度上尚不清楚。这篇综述旨在概述适应性免疫细胞（特别是 T 细胞）在纤维肌痛生理病理学中的作用。它还旨在将基础科学中出现的最新进展联系起来，以设想新的观点来解释 T 细胞在连接纤维肌痛的心理、神经和炎症症状中的作用。
