Shin Eui-Cheol, Seifert Ulrike, Kato Takanobu, Rice Charles M, Feinstone Stephen M, Kloetzel Peter-M, Rehermann Barbara
Immunology Section and Liver Diseases Branch, NIDDK, NIH, Department of Health and Human Services, Bethesda, Maryland 20892, USA.
J Clin Invest. 2006 Nov;116(11):3006-14. doi: 10.1172/JCI29832. Epub 2006 Oct 12.
IFN-gamma is known as the initial and primary inducer of immunoproteasomes during viral infections. We now report that type I IFN induced the transcription and translation of immunoproteasome subunits, their incorporation into the proteasome complex, and the generation of an immunoproteasome-dependent CD8 T cell epitope in vitro and provide in vivo evidence that this mechanism occurs prior to IFN-gamma responses at the site of viral infection. Type I IFN-mediated generation of immunoproteasomes was initiated by either poly(I:C) or HCV RNA in human hepatoma cells and was inhibited by neutralization of type I IFN. In serial liver biopsies of chimpanzees with acute HCV infection, increases in immunoproteasome subunit mRNA preceded intrahepatic IFN-gamma responses by several weeks, instead coinciding with intrahepatic type I IFN responses. Thus, viral RNA-induced innate immune responses regulate the antigen-processing machinery, which occurs prior to the detection of IFN-gamma at the site of infection. This mechanism may contribute to the high effectiveness (95%) of type I IFN-based therapies if administered early during HCV infection.
干扰素-γ被认为是病毒感染期间免疫蛋白酶体的初始和主要诱导剂。我们现在报告,I型干扰素在体外诱导免疫蛋白酶体亚基的转录和翻译、它们并入蛋白酶体复合物以及产生免疫蛋白酶体依赖性CD8 T细胞表位,并提供体内证据表明这种机制在病毒感染部位的干扰素-γ反应之前就已发生。I型干扰素介导的免疫蛋白酶体生成在人肝癌细胞中由聚肌苷酸胞苷酸(poly(I:C))或丙型肝炎病毒(HCV)RNA启动,并被I型干扰素的中和所抑制。在急性HCV感染的黑猩猩的系列肝活检中,免疫蛋白酶体亚基mRNA的增加比肝内干扰素-γ反应提前数周,反而与肝内I型干扰素反应一致。因此,病毒RNA诱导的先天免疫反应调节抗原加工机制,这在感染部位检测到干扰素-γ之前就已发生。如果在HCV感染早期给药,这种机制可能有助于基于I型干扰素的疗法的高有效性(95%)。