IMMUNOLOGICAL ABNORMALITIES IN CHRONIC FATIGUE SYNDROME
IMMUNOLOGICAL ABNORMALITIES IN CHRONIC FATIGUE SYNDROME
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DOI：
10.1128/jcm.28.6.1403-1410.1990
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发表时间：
1990-06-01
影响因子：
9.4
通讯作者：
FLETCHER, MA
中科院分区：
文献类型：
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作者：
KLIMAS, NG;SALVATO, FR;FLETCHER, MA
慢性疲劳综合征（CFS），以前称为慢性爱泼斯坦-巴尔病毒综合征，是一种复杂且病因不确定的临床状态。为了全面表征与该综合征患者细胞免疫功能相关的实验室标志物的状况，我们研究了30例临床定义为CFS的患者。所有的研究对象都发现这些标记物有多种异常。与正常对照相比，在这些患者中检测到的最一致的免疫异常是低自然杀伤（NK）细胞毒性。NK细胞的数量，通过与单克隆抗体NKH的反应性来确定。I （cd56）升高，但每cd56细胞对K562肿瘤细胞的杀伤作用明显降低。与正常对照组相比，大多数患者在植物血凝素和美洲商陆有丝分裂原刺激后的淋巴细胞增殖反应减少，有丝分裂原刺激后γ干扰素的产生也减少。外周血淋巴细胞表型标记分析显示，CFS患者与对照组存在显著差异。抑制细胞毒性T淋巴细胞CD8的百分比增加，表达II类激活标记的CD8细胞的数量按比例增加。大多数患者表达活化标志物CDw26的CD2细胞数量升高。CFS患者的CD4细胞数量和CD4+CD29+辅助亚群的数量与对照组无明显差异。然而，CD4+ CD45RA+细胞的抑制诱导剂亚群显著减少。B细胞CD20和CD21的数量升高，同时，共表达CD20和CD5的B细胞亚群的数量也升高。观察到的免疫标记物异常模式与慢性病毒再激活综合征相一致。
The chronic fatigue syndrome (CFS), formerly known as chronic Epstein-Barr virus syndrome, is a clinical state of some complexity and uncertain etiology. In order to characterize in a comprehensive manner the status of laboratory markers associated with cellular immune function in patients with this syndrome, 30 patients with clinically defined CFS were studied. All of the subjects were found to have multiple abnormalities in these markers. The most consistent immunological abnormality detected among these patients, when compared with normal controls, was low natural killer (NK) cell cytotoxicity. The number of NK cells, as defined by reactivity with monoclonal antibody NKH. I (CD 56) was elevated, but the killing of K562 tumor cells per CD 56 cell was significantly diminished. Lymphoproliferative responses after stimulation with phytohemagglutinin and pokeweed mitogen were decreased in most patients when compared with those in normal controls, as was the production of gamma interferon following mitogen stimulation. Lymphocyte phenotypic marker analysis of peripheral blood lymphocytes showed that there were significant differences between patients with CFS and controls. There was an increase in the percentage of suppressor-cytotoxic T lymphocytes, CD8, and a proportionally larger increase in the number of CD8 cells expressing the class II activation marker. Most patients had an elevated number of CD2 cells which expressed the activation marker CDw26. The numbers of CD4 cells and the helper subset of CD4+CD29+ cells in patients with CFS were not different from those in controls. There was, however, a significant decrease in the suppressor inducer subset of CD4+ CD45RA+ cells. The numbers of B cells, CD20 and CD21, were elevated, as were the numbers of a subset of B cells which coexpressed CD20 and CD5. The pattern of immune marker abnormalities observed was compatible with a chronic viral reactivation syndrome.