Shao-Hsien C, Lang I, Gunn H, Lydyard P
Transplantation. 1983 Feb;35(2):127-9. doi: 10.1097/00007890-198302000-00004.
Concentrations of 0.1 to 10.0 micrograms of cyclosporin A (Cy A) per ml do not directly inhibit the lysis of 51Cr-labeled K562 target cells by human peripheral blood natural killer (NK) cells nor of antibody-coated chicken red blood cells by antibody-dependent cellular cytotoxicity (ADCC) effector cells. Pretreatment of effector cells with Cy A for 18 hr still failed to affect NK or ADCC effector function. However, induction of NK cell activity by overnight pretreatment of effector cells by polyinosinate-polycytidylate (PolyIC) is inhibited by as little as 1 micrograms of Cy A per ml. The mechanism of inhibition may involve a direct effect of Cy A on "induced" or "activated" NK cells or inhibition of the release of Poly IC-induced interferon from lymphocytes.
每毫升含0.1至10.0微克环孢素A(Cy A)的浓度不会直接抑制人外周血自然杀伤(NK)细胞对51铬标记的K562靶细胞的裂解,也不会抑制抗体依赖性细胞毒性(ADCC)效应细胞对抗体包被的鸡红细胞的裂解。用Cy A对效应细胞进行18小时的预处理仍无法影响NK或ADCC效应功能。然而,每毫升低至1微克的Cy A就能抑制通过聚肌苷酸-聚胞苷酸(PolyIC)对效应细胞进行过夜预处理所诱导的NK细胞活性。抑制机制可能涉及Cy A对“诱导的”或“活化的”NK细胞的直接作用,或抑制淋巴细胞释放Poly IC诱导的干扰素。