Sun A, Chu C T, Wu Y C, Yuan J H
School of Dentistry, College of Medicine, National Taiwan University, Taipei, Republic of China.
Clin Immunol Immunopathol. 1991 Jul;60(1):83-92. doi: 10.1016/0090-1229(91)90114-p.
Natural killer (NK) cell activity was studied serially in the peripheral blood obtained from 35 patients with recurrent aphthous ulcers (RAU) and from 46 age/sex-matched normal healthy controls. The NK cell activity was assayed by a 4-hr 51Cr release assay using K562 cells as targets. The results showed that the patients in remission (2 weeks of convalesence) had normal NK cell activity compared to that of normal controls. Four stages of evolution (early, exacerbation, postexacerbation, and convalescence) in these patients were further evaluated. Increased NK cell activity in the exacerbation of major aphthous ulcer was noted. In contrast, depressed NK cell activity in postexacerbation and in 1 week of convalescence was found at different effector/target (E/T) ratios. The depressed NK cell activity was interpreted as temporary and a secondary phenomenon in the immunopathogenesis of this disease. Partial restoration of depressed NK cell activity by adding recombinant interleukin-2 (rIL-2) suggests that other factors are also involved in the process or that IL-2 deficiency exists in RAU patients. However, no deficiency of plasma IL-2 and interferon-gamma (IFN-gamma) was noted. The percentage of large granular lymphocytes (LGL, NK/K) was correlated with NK cell activity, with both parameters being depressed in the postexacerbation of RAU patients. NK cell activity of RAU patients was still depressed after the depletion of plastic adherent cells. Suprisingly, in contrast to the remission stage, unresponsiveness to rIL-2 of normal NK cell activity in the exacerbation stage was found. The discrepancy was not associated with different subpopulations of NK heterogeneous cells. Immunopathogenesis of RAU on the NK-IFN-IL-2-IL-2R system needs further clarification.
对35例复发性阿弗他溃疡（RAU）患者及46名年龄和性别匹配的正常健康对照者外周血中的自然杀伤（NK）细胞活性进行了连续研究。采用以K562细胞为靶细胞的4小时51Cr释放试验检测NK细胞活性。结果显示，缓解期（恢复期2周）患者的NK细胞活性与正常对照者相比正常。对这些患者的四个演变阶段（早期、加重期、加重后期和恢复期）进行了进一步评估。注意到在重型阿弗他溃疡加重期NK细胞活性增加。相反，在加重后期和恢复期1周时，在不同的效应细胞/靶细胞（E/T）比例下发现NK细胞活性降低。NK细胞活性降低被解释为该病免疫发病机制中的一种暂时的继发性现象。添加重组白细胞介素-2（rIL-2）后，降低的NK细胞活性部分恢复，这表明该过程中还涉及其他因素，或者RAU患者存在IL-2缺乏。然而，未发现血浆IL-2和干扰素-γ（IFN-γ）缺乏。大颗粒淋巴细胞（LGL，NK/K）百分比与NK细胞活性相关，在RAU患者加重后期这两个参数均降低。去除塑料黏附细胞后，RAU患者的NK细胞活性仍然降低。令人惊讶的是，与缓解期相比，在加重期正常NK细胞活性对rIL-2无反应。这种差异与NK异质性细胞的不同亚群无关。RAU在NK-IFN-IL-2-IL-2R系统上的免疫发病机制需要进一步阐明。
