Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on antiviral activity and (2'-5') oligo (A) synthetase induction in a myelomonocytic cell line.
Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on antiviral activity and (2'-5') oligo (A) synthetase induction in a myelomonocytic cell line.
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干扰素-γ 和肿瘤坏死因子-α 对骨髓单核细胞系中抗病毒活性和 (2-5) 寡 (A) 合成酶诱导的协同作用。
DOI：
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发表时间：
1990
影响因子：
5.5
通讯作者：
R. Falcoff
中科院分区：
文献类型：
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作者：
J. Wietzerbin;C. Gaudelet;L. Catinot;J. Chebath;R. Falcoff
未观察到TNF对HL60或U937细胞有抗病毒作用。然而，它确实显著增强干扰素(IFN)- γ介导的U937细胞的抗病毒活性。用ifn - γ增强（2'-5'）寡核苷酸(A)合成酶活性（2.5倍），而用TNF治疗则没有。联合tnf - α + ifn - γ治疗可显著提高这种活性（20-40倍）。这种增加与U937细胞中（2’-5’）寡聚(A)合成酶mRNA水平的大幅增加有关。在HL60细胞中没有观察到这种作用。此外，结合研究和交联分析表明，ifn - γ在U937细胞中调节tnf - α受体而不改变其性质，但在HL60细胞中没有这样做。
TNF was not observed to have an antiviral effect on either HL60 or U937 cells. However, it did significantly enhance interferon (IFN)-gamma-mediated antiviral activity in U937 cells. Treatment of U937 cells with IFN-gamma enhanced (2'-5') oligo (A) synthetase activity (2.5-fold) but treatment with TNF did not. Combined treatment with TNF-alpha + IFN-gamma increased this activity dramatically (20-40-fold). This increase correlated with the very large increase in the (2'-5') oligo (A) synthetase mRNA level in U937 cells. No such effects were observed in HL60 cells. Furthermore, binding studies and cross-linking analysis showed that IFN-gamma modulated TNF-alpha receptors in U937 cells without altering their properties, but did not do so in HL60 cells.