论文部分内容阅读
通过观察20例正常人和24例消化系恶性肿瘤病人外周血自然杀伤细胞(NK)和淋巴因子激活的杀伤细胞(LAK)的活性变化,以及加用重组白细胞介素2(rIL-2)刺激前后T淋巴细胞表型变化。结果发现肿瘤病人的NK细胞活性明显下降,但经rIL-2激活后LAK细胞活性得到明显提高,其溶解率接近正常水平。肿瘤病人的总T淋巴细胞(CD_(3+))和辅助/诱导T淋巴细胞(CD_(4+))水平低于正常,但抑制/杀伤淋巴细胞(CD_(8+))水平正常。辅助/诱导淋巴细胞与抑制/杀伤淋巴细胞之比为1.18,低于正常水平(1.55)。经加入rIL-2培养后,CD_(3+)和CD_(8+)淋巴细胞的比率明显升高并达正常水平。而在正常人此变化不明显,且加用rIL-2培养与不加者无显著差异。IL-2受体的表达正常人与肿瘤病人无异。结果显示胃肠道恶性肿瘤病人的免疫机制受到抑制,但能被IL-2提高至正常水平。
The activity of natural killer cells (NK) and lymphokine-activated killer cells (LAK) in peripheral blood from patients with 20 normal controls and 24 patients with digestive malignancy was observed, as well as stimulation with recombinant interleukin 2 (rIL-2). Before and after T lymphocyte phenotype changes. The results showed that the NK cell activity of tumor patients decreased significantly, but the activity of LAK cells was significantly increased after rIL-2 activation, and the dissolution rate was close to normal. The total T-lymphocytes (CD_(3+)) and helper/inducible T-lymphocytes (CD_(4+)) levels of cancer patients were lower than normal, but the levels of suppressor/lymphocyte (CD_(8+)) were normal. The ratio of helper/inducing lymphocytes to killer/killer lymphocytes was 1.18, which was lower than normal (1.55). After incubation with rIL-2, the ratio of CD3+ and CD8+ lymphocytes increased significantly and reached normal levels. However, this change was not significant in normal subjects, and there was no significant difference between the addition of rIL-2 culture and non-addition. The normal expression of IL-2 receptor is no different from that of cancer patients. The results showed that the immune mechanism of patients with gastrointestinal cancers was inhibited but could be elevated to normal levels by IL-2.