Minato N, Takeda A, Kano S, Takaku F
J Clin Invest. 1982 Mar;69(3):581-8. doi: 10.1172/jci110484.
The natural killer (NK)-interferon (IFN) system is shown to be significantly involved in the resistance of host to viral infections and to tumours in numbers of animal models (1-4). The patients with Sjögren syndrome (SS) as well as those with collagen diseases were systematically investigated for the functions of NK-IFN system, including endogenous and augmented NK activity, IFN production, and responsiveness of NK cells to IFN stimulation, using virus persistently infected cells (heLa-measles cells) as target and stimulator cells. Although endogenous NK activity was not reduced, augmented NK activity by HeLa-measles cells in vitro was significantly depressed in patients with SS compared with that in age-matched normal controls. The patients with SS had also impaired capacity to produce IFN, which is shown to be a major factor regulating NK activity (5,6) in response to HeLa-measles cells in vitro. In three patients with SS who showed severely depressed NK activity, the effect of exogenous IFN was examined, and virtually no augmentation of NK activity was observed in all cases. Under the same condition, the normal controls demonstrated a dramatic increase in NK activity. The reduced IFN production was observed in all examined patients with SS, whereas impaired augmentation of NK activity by the stimulation with HeLa-measles cells as well as IFN seemed to be more striking in patients with the systemic manifestations of the disease, such as hypergammaglobulinemia and lymphoid hyperplasia. The possible involvement of dysfunction of NK-IFN system in the systemic manifestations of SS is discussed.
在许多动物模型中，自然杀伤（NK）-干扰素（IFN）系统被证明在宿主抵抗病毒感染和肿瘤方面发挥着重要作用（1-4）。我们使用持续感染病毒的细胞（HeLa-麻疹细胞）作为靶细胞和刺激细胞，对干燥综合征（SS）患者以及胶原病患者的NK-IFN系统功能进行了系统研究，包括内源性和增强后的NK活性、IFN产生以及NK细胞对IFN刺激的反应性。虽然内源性NK活性没有降低，但与年龄匹配的正常对照组相比，SS患者体外经HeLa-麻疹细胞增强后的NK活性明显降低。SS患者产生IFN的能力也受损，IFN被证明是体外调节NK活性的主要因素（5,6），在SS患者中，IFN产生能力受损，在体外对HeLa-麻疹细胞的反应中，IFN产生能力受损。在3例NK活性严重降低的SS患者中，检测了外源性IFN的作用，所有病例均未观察到NK活性的增强。在相同条件下，正常对照组的NK活性显著增加。在所有检测的SS患者中均观察到IFN产生减少，而在患有疾病全身表现（如高球蛋白血症和淋巴组织增生）且受到HeLa-麻疹细胞及IFN刺激后NK活性增强受损的患者中，这种情况似乎更为明显。本文讨论了NK-IFN系统功能障碍可能参与SS全身表现的情况。
