Immunological aspects of chronic fatigue syndrome
Immunological aspects of chronic fatigue syndrome
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DOI：
10.1016/j.autrev.2008.08.003
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发表时间：
2009-02-01
影响因子：
13.6
通讯作者：
Ricevuti, Giovanni
中科院分区：
文献类型：
--
作者：
Lorusso, Lorenzo;Mikhaylova, Svetlana V.;Ricevuti, Giovanni
慢性疲劳综合征（CFS）是一种特殊的临床状况，其特征是不明原因的致残性疲劳和至少6个月的非特异性伴随症状的组合，在没有医学诊断的情况下，可以解释临床表现。其他常见症状包括头痛、肌痛、关节痛和运动后不适;认知困难，记忆力和注意力受损;睡眠不清醒;情绪变化。类似的疾病已经被描述了至少两个世纪，并被不同地命名为神经衰弱，病毒后疲劳，肌痛性脑脊髓炎和慢性单核细胞增多症。最近的纵向研究表明，一些受慢性疲劳综合征影响的人随着时间的推移而改善，但大多数人在几年内仍然功能受损。CFS的估计全球患病率为0.4-1%，在美国影响超过800，000人，在英国影响约240，000名患者。没有身体检查的迹象是特定的CFS和没有诊断测试确定这种综合征。CFS的病理生理机制尚不清楚。主要的假设包括对共同抗原的异常免疫反应导致的中枢神经系统功能改变;神经内分泌紊乱;有知觉的人对感染或其他刺激的反应导致的认知障碍。目前的概念是CFS发病机制是一个多因素的条件。各种研究都在寻找CFS患者免疫紊乱的证据。已经报道了细胞因子谱的改变、自然杀伤（NK）细胞的功能降低、自身抗体的存在以及T细胞对有丝分裂原和其他特异性抗原的应答降低。观察到的高水平的促炎细胞因子可以解释一些表现，如疲劳和流感样症状，并影响NK活性。已经描述了T淋巴细胞亚群的异常活化和抗体依赖性细胞介导的细胞毒性的降低。据报道，CD 8+细胞毒性T淋巴细胞和CD 38和HLA-DR活化标志物的数量增加，并观察到与CD 28 + T亚群表达增加相关的CD 11b表达降低。本文综述了CFS的免疫方面，并提供了一个免疫假说的疾病过程。(C)2008 Elsevier B. V.保留所有权利。
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 neuroenclocrine 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 flulike 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. (C) 2008 Elsevier B.V. All rights reserved.