Sibbitt W L, Froelich C J, Bankhurst A D
Arthritis Rheum. 1983 Dec;26(12):1452-9. doi: 10.1002/art.1780261206.
In the present study we examined one aspect of the derangement in natural cytotoxicity (natural killer, NK) activity observed in some patients with systemic lupus erythematosus (SLE), i.e., the lack of enhancement of NK activity usually seen with interferon (IFN). NK activity of SLE patients as a group was 23.0 +/- 3.9 lytic units (LU)/10(7) cells (mean +/- SE). This contrasted with the NK activity found in normal controls (45.0 +/- 3.8 LU/10(7) cells) (P less than 0.05). The enhancement seen with IFN was an increase of 15.4 +/- 4.0 LU/10(7) cells in SLE patients compared with 104.6 +/- 192 LU/10(7) cells in control subjects (P less than 0.05). SLE sera and aggregated IgG (Agg-IgG) also inhibited the increase in NK activity of normal peripheral blood mononuclear cells after IFN priming. The results reported here support the hypothesis that the impaired baseline NK activity and poor response to IFN noted in SLE are secondary, in part, to the presence of inhibitory serum factors and preactivation by IFN.
在本研究中,我们检测了系统性红斑狼疮(SLE)患者自然细胞毒性(自然杀伤细胞,NK)活性紊乱的一个方面,即通常在干扰素(IFN)作用下可观察到的NK活性增强缺失。SLE患者群体的NK活性为23.0±3.9溶细胞单位(LU)/10⁷细胞(均值±标准误)。这与正常对照组的NK活性(45.0±3.8 LU/10⁷细胞)形成对比(P<0.05)。SLE患者经IFN作用后活性增强为15.4±4.0 LU/10⁷细胞,而对照组为104.6±19.2 LU/10⁷细胞(P<0.05)。SLE血清和聚集的IgG(Agg-IgG)也抑制了IFN预处理后正常外周血单个核细胞NK活性的增强。此处报告的结果支持这样的假说,即SLE患者中观察到的基线NK活性受损及对IFN反应不佳,部分是由抑制性血清因子的存在以及IFN的预激活作用所致。