Author: Seo, Young-Jin; Hahm, Bumsuk
                    Title: Type I Interferon Modulates the Battle of Host Immune System Against Viruses  Cord-id: r6n6xgyr  Document date: 2010_8_26
                    ID: r6n6xgyr
                    
                    Snippet: Type I interferon (IFN), as its name implies, ‘interferes’ with virus replication by activating numerous genes. Further, virus-induced type I IFN regulates the magnitude and functions of cells directing the host immune system. Importantly, recent exploration into how type I IFN operates following virus infection has advanced our understanding of its role with respect to modulation of host innate and adaptive immune responses. Such activities include the activation of antigen-presenting dendr
                    
                    
                    
                     
                    
                    
                    
                    
                        
                            
                                Document: Type I interferon (IFN), as its name implies, ‘interferes’ with virus replication by activating numerous genes. Further, virus-induced type I IFN regulates the magnitude and functions of cells directing the host immune system. Importantly, recent exploration into how type I IFN operates following virus infection has advanced our understanding of its role with respect to modulation of host innate and adaptive immune responses. Such activities include the activation of antigen-presenting dendritic cells and the localization, expansion or differentiation of virus-specific T lymphocytes and antibody-producing B lymphocytes. However, type I IFN not only benefits the host but can also induce unnecessary or extremely pathogenic immune responses. This review focuses on such interactions and the manner in which type I IFN induces dynamic changes in the host immune network, particularly adaptive immune responses to viral invasion. Manipulating the type I IFN-mediated host immune response during virus infections could provide new immunotherapeutic interventions to remedy viral diseases and implement more effective and sustainable type I IFN therapy.
 
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