Pandita R, Pocsik E, Aggarwal B B
Department of Clinical Immunology and Biological Therapy, University of Texas M.D. Anderson Cancer Center, Houston 77030.
FEBS Lett. 1992 Nov 2;312(1):87-90. doi: 10.1016/0014-5793(92)81416-j.
Interferons are known to potentiate various biological effects of tumor necrosis factor (TNF). Recently, two different types of TNF receptors with molecular masses of 60 kDa (p60) and 80 kDa (p80), primarily expressed by epithelial cells and myeloid cells, respectively, have been identified. In the present report, we examined the effect of interferon-gamma (IFN-gamma) on each type of TNF receptor. Our results indicate that IFN-gamma induces TNF receptors on both myeloid (e.g. HL-60) and epithelial cells (e.g. HeLa). Furthermore, by using antibodies specific to each type of receptor, we demonstrate that both TNF receptors are equally inducible by IFN-alpha, IFN-beta and IFN-gamma. Thus, the increase in TNF receptors by interferons may play a role in their synergistic cellular response.
已知干扰素可增强肿瘤坏死因子(TNF)的多种生物学效应。最近,已鉴定出两种分子量分别为60 kDa(p60)和80 kDa(p80)的不同类型的TNF受体,它们分别主要由上皮细胞和髓样细胞表达。在本报告中,我们研究了γ干扰素(IFN-γ)对每种类型TNF受体的影响。我们的结果表明,IFN-γ可诱导髓样细胞(如HL-60)和上皮细胞(如HeLa)上的TNF受体。此外,通过使用针对每种受体类型的特异性抗体,我们证明两种TNF受体均可被IFN-α、IFN-β和IFN-γ同等程度地诱导。因此,干扰素引起的TNF受体增加可能在其协同细胞反应中起作用。