Lorusso Lorenzo, Mikhaylova Svetlana V, Capelli Enrica, Ferrari Daniela, Ngonga Gaelle K, Ricevuti Giovanni
Department of Neurology, Mellino Mellini Hospital, Chiari, Brescia, Italy.
Autoimmun Rev. 2009 Feb;8(4):287-91. doi: 10.1016/j.autrev.2008.08.003. Epub 2008 Sep 16.
Chronic fatigue syndrome (CFS) is a specific clinical condition that characterises unexplained disabling fatigue and a combination of non-specific accompanying symptoms for at least 6 months, in the absence of a medical diagnosis that would otherwise explain the clinical presentation. Other common symptoms include headaches, myalgia, arthralgia, and post-exertional malaise; cognitive difficulties, with impaired memory and concentration; unrefreshing sleep; and mood changes. Similar disorders have been described for at least two centuries and have been differently named neurasthenia, post-viral fatigue, myalgic encephalomyelitis and chronic mononucleosis. Recent longitudinal studies suggest that some people affected by chronic fatigue syndrome improve with time but that most remain functionally impaired for several years. The estimated worldwide prevalence of CFS is 0.4-1% and it affects over 800,000 people in the United States and approximately 240,000 patients in the UK. No physical examination signs are specific to CFS and no diagnostic tests identify this syndrome. The pathophysiological mechanism of CFS is unclear. The main hypotheses include altered central nervous system functioning resulting from an abnormal immune response against a common antigen; a neuroendocrine disturbance; cognitive impairment caused by response to infection or other stimuli in sentient people. The current concept is that CFS pathogenesis is a multifactorial condition. Various studies have sought evidence for a disturbance in immunity in people with CFS. An alteration in cytokine profile, a decreased function of natural killer (NK) cells, a presence of autoantibodies and a reduced responses of T cells to mitogens and other specific antigens have been reported. The observed high level of pro-inflammatory cytokines may explain some of the manifestations such as fatigue and flu-like symptoms and influence NK activity. Abnormal activation of the T lymphocyte subsets and a decrease in antibody-dependent cell-mediated cytotoxicity have been described. An increased number of CD8+ cytotoxic T lymphocytes and CD38 and HLA-DR activation markers have been reported, and a decrease in CD11b expression associated with an increased expression of CD28+ T subsets has been observed. This review discusses the immunological aspects of CFS and offers an immunological hypothesis for the disease processes.
慢性疲劳综合征（CFS）是一种特殊的临床病症，其特征为不明原因的致残性疲劳以及至少持续6个月的一系列非特异性伴随症状，且不存在能解释该临床表现的其他医学诊断。其他常见症状包括头痛、肌痛、关节痛和劳累后不适；认知困难，表现为记忆力和注意力受损；睡眠不能解乏；以及情绪变化。类似的病症至少已被描述了两个世纪，曾被赋予不同的名称，如神经衰弱、病毒感染后疲劳、肌痛性脑脊髓炎和慢性单核细胞增多症。近期的纵向研究表明，一些慢性疲劳综合征患者会随时间好转，但大多数患者在数年内仍存在功能障碍。据估计，慢性疲劳综合征在全球的患病率为0.4%-1%，在美国影响超过80万人，在英国约有24万患者。没有任何体格检查体征是慢性疲劳综合征所特有的，也没有诊断测试能确诊该综合征。慢性疲劳综合征的病理生理机制尚不清楚。主要假说包括针对常见抗原的异常免疫反应导致中枢神经系统功能改变；神经内分泌紊乱；有感知能力的人对感染或其他刺激的反应引起认知障碍。目前的观点是，慢性疲劳综合征的发病机制是一种多因素病症。各项研究都在寻找慢性疲劳综合征患者免疫功能紊乱的证据。已有报告称细胞因子谱改变、自然杀伤（NK）细胞功能下降、自身抗体的存在以及T细胞对丝裂原和其他特定抗原的反应降低。所观察到的促炎细胞因子水平升高可能解释了诸如疲劳和流感样症状等一些表现，并影响NK活性。已描述了T淋巴细胞亚群的异常激活以及抗体依赖性细胞介导的细胞毒性降低。有报告称CD8+细胞毒性T淋巴细胞以及CD38和HLA-DR激活标志物的数量增加，并且观察到与CD28+T亚群表达增加相关的CD11b表达减少。本综述讨论了慢性疲劳综合征的免疫学方面，并为疾病过程提供了一种免疫学假说。
