Kaudewitz P, Zander H, Abb J, Ziegler-Heitbrock H W, Riethmüller G
Hum Immunol. 1983 May;7(1):51-8. doi: 10.1016/0198-8859(83)90007-1.
A dysfunction in natural killer (NK) cell activity has been assumed to play a substantial role in the pathogenesis of multiple sclerosis (MS). To investigate whether such a defect is genetically determined and thus in combination with a certain HLA status may represent an additional risk factor for contracting MS, spontaneous and interferon (IFN) induced NK cells activity against the K562 target cell were analyzed in nine pairs of monozygotic twins discordant for MS. In addition, IFN production was tested in nonadherent lymphocytes stimulated with PHA, influenza virus or leukemia cells. When compared to healthy controls, NK function appeared to be normal in healthy twins, whereas some MS patient displayed decreased activity. No difference in IFN induced NK cell activity and IFN production could be detected between normal controls, healthy twins, and MS patients. These data argue against a genetically determined dysfunction within the NK-IFN system in patients with MS.
自然杀伤（NK）细胞活性障碍被认为在多发性硬化症（MS）的发病机制中起重要作用。为了研究这种缺陷是否由基因决定，以及因此与特定的人类白细胞抗原（HLA）状态相结合是否可能代表患MS的另一个风险因素，对9对患MS的单卵双胞胎进行了分析，检测了其自发和干扰素（IFN）诱导的针对K562靶细胞的NK细胞活性。此外，还检测了用植物血凝素（PHA）、流感病毒或白血病细胞刺激的非贴壁淋巴细胞中的IFN产生情况。与健康对照组相比，健康双胞胎的NK功能似乎正常，而一些MS患者的活性降低。在正常对照组、健康双胞胎和MS患者之间，未检测到IFN诱导的NK细胞活性和IFN产生的差异。这些数据表明，MS患者的NK-IFN系统中不存在由基因决定的功能障碍。
