Wattrang E, Cederblad B, Fossum C
Department of Veterinary Microbiology, Swedish University of Agricultural Sciences, Uppsala.
J Interferon Cytokine Res. 1995 Apr;15(4):301-8. doi: 10.1089/jir.1995.15.301.
The interaction between virus and peripheral blood mononuclear cells (PBMC) required to elicit the production of interferon-alpha (IFN-alpha) by the so-called natural interferon-producing cell is unknown. However, results from inhibition experiments suggest that viral glycoproteins are essential in this IFN induction process. We demonstrate here that cellular glycoproteins also appear to be involved in the initiation of IFN-alpha production. Lectins, that is, sugar binding glycoproteins, inhibited the Aujeszky's disease virus-induced IFN-alpha production of porcine PBMC by up to 99%. The level of inhibition varied with lectin used (concanavalin A, Galanthus nivalis lectin, Helix pomatia lectin, and lentil lectin). Preincubation experiments with porcine cells and concanavalin A (ConA) revealed that the lectin exerted its major effect directly on the PBMC. Although the IFN-alpha production in some cases was reduced by more than 90%, the PBMC were still able to proliferate in response to mitogenic lectins. The ConA-mediated inhibition of the IFN-alpha production was reduced if the lectin was added later than 6-8 h after the start of induction and was not mediated by soluble factors. Both orthovanadate and staurosporine inhibited the IFN-alpha production and did not relieve the ConA-mediated inhibition. Thus, ConA seems to interfere with the early events during IFN-alpha induction, but the mechanisms behind this interference could not be clarified.
引发所谓的天然干扰素产生细胞产生α干扰素(IFN-α)所需的病毒与外周血单个核细胞(PBMC)之间的相互作用尚不清楚。然而,抑制实验结果表明病毒糖蛋白在这种IFN诱导过程中至关重要。我们在此证明细胞糖蛋白似乎也参与了IFN-α产生的起始过程。凝集素,即糖结合糖蛋白,可将奥耶斯基氏病病毒诱导的猪PBMC的IFN-α产生抑制高达99%。抑制水平因所用凝集素(伴刀豆球蛋白A、雪花莲凝集素、蜗牛凝集素和扁豆凝集素)而异。用猪细胞和伴刀豆球蛋白A(ConA)进行的预孵育实验表明,凝集素主要直接作用于PBMC。尽管在某些情况下IFN-α产生减少了90%以上,但PBMC仍能够对促有丝分裂凝集素作出增殖反应。如果凝集素在诱导开始后6 - 8小时后添加,则ConA介导的IFN-α产生抑制作用会降低,且该抑制作用不是由可溶性因子介导的。原钒酸盐和星形孢菌素均抑制IFN-α产生,且不能缓解ConA介导的抑制作用。因此,ConA似乎干扰了IFN-α诱导过程中的早期事件,但这种干扰背后的机制尚不清楚。