Towata T, Hayashi N, Katayama K, Takehara T, Miyoshi E, Kawanishi Y, Ueda K, Kasahara A, Fusamoto H, Kamada T
First Department of Medicine, Osaka University Medical School, Japan.
Gastroenterol Jpn. 1993 Apr;28(2):242-8. doi: 10.1007/BF02779226.
This study investigated the expression of HLA class I antigens on Huh6 and HB611 cells induced by interferon (IFN)-alpha, IFN-gamma, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta. All of these cytokines induced the antigens on both cells in a dose-dependent manner, with IFNs inducing much more expression than TNF-alpha or IL-1 beta. We have already reported that protein kinase C (PKC) is involved in the antigen expression induced by IFN-gamma on Huh6 cells. The antigen expression induced by IFN-alpha was also blocked by a PKC inhibitor, H-7. However, the antigen expression by TNF-alpha or IL-1 beta was not inhibited by H-7, by a protein kinase A inhibitor, HA1004, nor by a calmodulin antagonist, W-7. These results suggested that PKC, Ca(2+)-calmodulin, and cAMP are not involved in the induction of HLA class I antigens on both cells by TNF-alpha and IL-1 beta. We concluded that TNF-alpha and IL-1 beta induced much less expression of HLA class I antigens on both cells than IFNs and that this might be because the signaling pathway by TNF-alpha and IL-1 beta differed from that by IFNs.
本研究调查了α干扰素(IFN-α)、γ干扰素(IFN-γ)、肿瘤坏死因子(TNF-α)和白细胞介素(IL)-1β诱导下,Huh6细胞和HB611细胞上HLA I类抗原的表达情况。所有这些细胞因子均以剂量依赖方式诱导两种细胞上的抗原表达,其中IFN诱导的表达量远高于TNF-α或IL-1β。我们之前已经报道过蛋白激酶C(PKC)参与IFN-γ诱导的Huh6细胞抗原表达。IFN-α诱导的抗原表达也被PKC抑制剂H-7所阻断。然而,TNF-α或IL-1β诱导的抗原表达不受H-7、蛋白激酶A抑制剂HA1004或钙调蛋白拮抗剂W-7的抑制。这些结果表明,PKC、Ca(2+)-钙调蛋白和环磷酸腺苷(cAMP)不参与TNF-α和IL-1β诱导两种细胞上HLA I类抗原的过程。我们得出结论,TNF-α和IL-1β诱导两种细胞上HLA I类抗原的表达量远低于IFN,这可能是因为TNF-α和IL-1β的信号通路与IFN不同。