作者: Emilio Yángüez , Alicia García-Culebras , Aldo Frau , Catalina Llompart , Klaus-Peter Knobeloch
DOI: 10.1371/JOURNAL.PPAT.1003632
关键词: Cytokine 、 Immune system 、 ISG15 、 Protein kinase B 、 Immunology 、 Cell biology 、 Interferon gamma 、 Macrophage 、 Biology 、 Interferon 、 Viral replication 、 Genetics 、 Molecular biology 、 Microbiology 、 Parasitology 、 Virology
摘要: Upon viral infection, the production of type I interferon (IFN) and subsequent upregulation IFN stimulated genes (ISGs) generate an antiviral state with important role in activation innate adaptive host immune responses. The ubiquitin-like protein (UBL) ISG15 is a critical IFN-induced molecule that protects against several infections, but mechanism by which exerts its function not completely understood. Here, we report plays regulation macrophage ISG15−/− macrophages display reduced activation, phagocytic capacity programmed cell death response to vaccinia virus (VACV) infection. Moreover, peritoneal from mice lacking are neither able phagocyte infected cells nor block infection co-culture experiments VACV-infected murine embryonic fibroblast (MEFs). This phenotype independent cytokine secretion, clearly correlates impaired kinase AKT knock-out (KO) macrophages. Altogether, these results indicate essential cellular point out better understanding responses triggered may lead development therapies human pathogens.