Rosenthal L A, Klyczek K K, Blank K J
University of Pennsylvania, Philadelphia 19104.
J Interferon Res. 1992 Dec;12(6):403-10. doi: 10.1089/jir.1992.12.403.
The constitutively class I-negative tumor cell line, Kgv, expresses H-2Dk in response to interferon-gamma (IFN-gamma), but not in response to IFN-alpha/beta, tumor necrosis factor, or lymphotoxin. H-2Dk expression was not induced on Kgv cells by the methylxanthines, pentoxifylline (PTX) and caffeine, which modulate class I expression on cells that constitutively express class I molecules. Treatment of Kgv cells with either IFN-alpha/beta, PTX, caffeine, or dibutyryl cAMP and a concentration of IFN-gamma insufficient by itself to induce Dk expression resulted in the induction of Dk expression. Since PTX and caffeine are cAMP-specific phosphodiesterase inhibitors, it is possible that the effects of PTX, caffeine, and dibutyryl cAMP involve a cAMP-dependent mechanism. We conclude that concentrations of IFN-gamma insufficient to induce Dk expression on Kgv cells may be capable of rendering the Dk gene responsive to signals that, in the absence of IFN-gamma treatment, have no effect on Dk expression.
组成型I类阴性肿瘤细胞系Kgv在受到γ干扰素（IFN-γ）刺激时表达H-2Dk，但对α/β干扰素、肿瘤坏死因子或淋巴毒素无反应。甲基黄嘌呤、己酮可可碱（PTX）和咖啡因可调节组成型表达I类分子的细胞上的I类表达，但它们不会在Kgv细胞上诱导H-2Dk表达。用α/β干扰素、PTX、咖啡因或二丁酰环磷腺苷（dibutyryl cAMP）处理Kgv细胞，再加上单独使用不足以诱导Dk表达的一定浓度的IFN-γ，会导致Dk表达的诱导。由于PTX和咖啡因是cAMP特异性磷酸二酯酶抑制剂，PTX、咖啡因和二丁酰环磷腺苷的作用可能涉及一种cAMP依赖性机制。我们得出结论，在Kgv细胞上不足以诱导Dk表达的IFN-γ浓度可能能够使Dk基因对某些信号产生反应，而这些信号在未用IFN-γ处理时对Dk表达没有影响。
