Barcova M, Kacani L, Speth C, Dierich M P
Institute for Hygiene, University of Innsbruck and Ludwig-Boltzmann-Institute for AIDS Research, Austria.
J Infect Dis. 1998 Apr;177(4):905-13. doi: 10.1086/515230.
The effect of extracellular domain of human immunodeficiency virus (HIV-1) transmembrane glycoprotein gp41 on interleukin (IL)-10, IL-2, interferon (IFN)-y, IL-4, and tumor necrosis factor-alpha production by human peripheral blood mononuclear cells (PBMC) was assessed by ELISA. Rapid gp41-induced increase of IL-10 production was detected in resting PBMC and isolated monocytes but not in B, T, or NK cells. Furthermore, gp41 also enhanced IL-10 production in staphylococcal enterotoxin B-stimulated PBMC, while synthesis of IL-2, IFN-gamma, and IL-4 in these cells was down-modulated. Kinetic studies revealed that increased IL-10 production preceded reduction of IL-2, indicating the possible IL-10 regulatory role in the gp41-induced down-modulation of this cytokine. Anti-IL-10 antibody reversed almost completely the gp41 inhibitory effect on IL-2 production. In this study, HIV-1 gp41 was a potent modulator of cytokine production by PBMC, in particular by increasing IL-10 secretion from normal monocytes/macrophages and consequently down-regulating IL-2 and IFN-gamma.
通过酶联免疫吸附测定法（ELISA）评估了人类免疫缺陷病毒（HIV-1）跨膜糖蛋白gp41的细胞外结构域对人外周血单个核细胞（PBMC）产生白细胞介素（IL）-10、IL-2、干扰素（IFN）-γ、IL-4和肿瘤坏死因子-α的影响。在静息的PBMC和分离的单核细胞中检测到gp41迅速诱导IL-10产生增加，但在B细胞、T细胞或自然杀伤（NK）细胞中未检测到。此外，gp41还增强了葡萄球菌肠毒素B刺激的PBMC中IL-10的产生，而这些细胞中IL-2、IFN-γ和IL-4的合成则被下调。动力学研究表明，IL-10产生增加先于IL-2减少，这表明IL-10在gp41诱导的该细胞因子下调中可能具有调节作用。抗IL-10抗体几乎完全逆转了gp41对IL-2产生的抑制作用。在本研究中，HIV-1 gp41是PBMC细胞因子产生的有效调节剂，特别是通过增加正常单核细胞/巨噬细胞分泌IL-10，从而下调IL-2和IFN-γ。
