Shin Eui-Cheol, Seifert Ulrike, Urban Sabrina, Truong Kim-Thuy, Feinstone Stephen M, Rice Charles M, Kloetzel Peter-M, Rehermann Barbara
Immunology Section, Liver Diseases Branch, NIDDK, National Institutes of Health, DHHS, Bethesda, MD 20892, USA.
J Interferon Cytokine Res. 2007 Dec;27(12):985-90. doi: 10.1089/jir.2007.0039.
Many components of the class I antigen-processing pathway are thought to be regulated solely by interferon-gamma (IFN-gamma). Herein, we report type I IFN-mediated induction of proteasome activator (PA28) subunits alpha and beta, endoplasmic reticulum aminopeptidase 1 (ERAP1), ERAP2, and leucine aminopeptidase (LAP). This mechanism was initiated by either synthetic RNA (poly(I-C)) or by hepatitis C virus (HCV) RNA-mediated induction of type I IFN and abrogated by blocking of type I IFN. In serial liver biopsies of chimpanzees with acute HCV infection, increases in PA28 subunit and aminopeptidase mRNA levels correlated with intrahepatic type I IFN responses and preceded intrahepatic IFN-gamma responses by several weeks. Thus, viral RNA-induced type I IFN regulates the antigen-processing machinery early during viral infection and prior to IFN-gamma response. This mechanism may contribute to the high effectiveness of type I IFN-based therapies if administered early during acute HCV infection.
I类抗原加工途径的许多成分被认为仅受γ干扰素(IFN-γ)调节。在此,我们报告I型干扰素介导的蛋白酶体激活剂(PA28)亚基α和β、内质网氨肽酶1(ERAP1)、ERAP2和亮氨酸氨肽酶(LAP)的诱导。该机制由合成RNA(聚肌胞苷酸)或丙型肝炎病毒(HCV)RNA介导的I型干扰素诱导启动,并通过阻断I型干扰素而消除。在急性HCV感染的黑猩猩的系列肝活检中,PA28亚基和氨肽酶mRNA水平的增加与肝内I型干扰素反应相关,并在肝内IFN-γ反应之前数周出现。因此,病毒RNA诱导的I型干扰素在病毒感染早期且在IFN-γ反应之前调节抗原加工机制。如果在急性HCV感染早期给予,这种机制可能有助于基于I型干扰素的治疗的高效性。