Herman J, Kew M C, Rabson A R
Cancer Immunol Immunother. 1985;19(2):148-53. doi: 10.1007/BF00199724.
Large granular lymphocytes (LGLs) from patients with malignant disease and from controls were activated by endotoxin or K562 cells, and the supernatants assayed for interleukin-1 (IL-1) activity. Normal LGLs produced significant amounts of IL-1, the activity of which could be neutralized by anti-human IL-1 antiserum. In patients with advanced cancer depressed IL-1 production was observed, which generally correlated with the degree of cytotoxicity produced by the LGLs. Prior treatment of the LGLs with interferon increased production of IL-1 by both control and patient cells. It is suggested that LGLs coming into contact with K562 cells produce IL-1, which is important in the effector-target cell interaction. The decreased cytotoxic activity of LGLs from cancer patients could be related to a defect in IL-1 production, an effect which can be partially corrected by in vitro interferon treatment.
来自恶性疾病患者和对照组的大颗粒淋巴细胞(LGL)被内毒素或K562细胞激活,然后检测其培养上清液中的白细胞介素-1(IL-1)活性。正常LGL可产生大量IL-1,其活性可被抗人IL-1抗血清中和。在晚期癌症患者中,观察到IL-1产生减少,这通常与LGL产生的细胞毒性程度相关。用干扰素预先处理LGL可增加对照组和患者组细胞的IL-1产生。有人提出,与K562细胞接触的LGL会产生IL-1,这在效应细胞与靶细胞的相互作用中很重要。癌症患者LGL的细胞毒性活性降低可能与IL-1产生缺陷有关,体外干扰素治疗可部分纠正这种效应。