Zippel D, Lackovic V, Kocisková D, Rovenský J, Borecký L, Stelzner A
Central Institute for Microbiology and Experimental Therapy, Academy of Sciences of the G.D.R., Jena.
Acta Virol. 1989 Sep;33(5):447-53.
Macrophage (MO) and natural killer (NK) cell mediated cytotoxicity to K562 target cells were strikingly decreased in patients with systemic lupus erythematosus (SLE). SLE NK cells failed to release soluble factor(s) for lysing the targets. IFN-induced enhancement of both types of cytotoxicity was impaired. NK cells from healthy subjects kept their activity in culture with or without IFN for more than six days whereas SLE NK cell activity declined to zero at day 3. So, the increased IFN level of many SLE patients and a possible prior IFN priming effect seemed unrelated to the insensitivity to exogenous IFN in vitro. Inhibition factor(s) of SLE serum suppressed NK cytotoxicity in the presence of IFN whereas IFN sensitivity of MO remained unaffected indicating the complex regulation by serum components of immune reactions.
系统性红斑狼疮(SLE)患者中,巨噬细胞(MO)和自然杀伤(NK)细胞对K562靶细胞的细胞毒性显著降低。SLE患者的NK细胞无法释放溶解靶细胞的可溶性因子。干扰素诱导的这两种细胞毒性增强均受损。健康受试者的NK细胞在有或无干扰素的培养中可保持活性超过6天,而SLE患者的NK细胞活性在第3天降至零。因此,许多SLE患者体内升高的干扰素水平以及可能的先前干扰素预激效应似乎与体外对外源性干扰素不敏感无关。SLE血清中的抑制因子在有干扰素存在时抑制NK细胞毒性,而MO对干扰素的敏感性不受影响,这表明免疫反应的血清成分具有复杂的调节作用。