Cseuz R, Panayi G S
Division of Medicine, United Medical School, Guy's Hospital, London.
Br J Rheumatol. 1990 Oct;29(5):358-62. doi: 10.1093/rheumatology/29.5.358.
Treatment with azathioprine of patients with rheumatoid arthritis leads to a dramatic reduction in the 4 h NK cytotoxicity against K562 cells. The 24 h cytotoxicity against K562 and U937 cells, however, remains intact. The generation of cell-free supernatant cytotoxic factor(s) after incubating non-adherent mononuclear cells with U937 cells for 24 h is similar in the azathioprine patients and the controls. A large part of this supernatant cytotoxicity is due to tumour necrosis factor alpha which can be inhibited by a specific monoclonal antibody. The mechanism of the reduced 4 h NK cytotoxicity remains unknown but is probably not related to the anti-inflammatory properties of azathioprine.
用硫唑嘌呤治疗类风湿性关节炎患者会导致对K562细胞的4小时自然杀伤细胞（NK）细胞毒性显著降低。然而，对K562和U937细胞的24小时细胞毒性保持不变。在将非贴壁单核细胞与U937细胞孵育24小时后，无细胞上清液细胞毒性因子的产生在硫唑嘌呤治疗的患者和对照组中相似。这种上清液细胞毒性的很大一部分归因于肿瘤坏死因子α，其可被特异性单克隆抗体抑制。4小时NK细胞毒性降低的机制尚不清楚，但可能与硫唑嘌呤的抗炎特性无关。
