As the first line of host defense against invading pathogens, the innate immune response is crucial to protect the host from viral infections. Interferons (IFNs) have been shown to be the most important defenders of innate immune system. There are three types of IFNs. Type I IFNs include IFN-a, IFN-ß, and a few other subtypes, and are produced by most cell types. Type II IFN includes only IFN-?, whose production is restricted to activated T cells, natural killer cells, and macrophages. Type III IFNs comprise IFN-?1, IFN-?2, IFN-?3, and IFN-?4, which are mainly produced by epithelial cells and dendritic cells. Host pattern recognition receptors (PRRs), including Toll-like receptors (TLRs) and RIG (retinoic-acid-inducible gene)-I-like receptors (RLRs), recognize specific pathogen-associated molecular patterns (PAMPs), which are generally viral RNA or DNA. Activation of TLR and RLR signaling pathways leads to activation of interferon regulatory factor 3 (IRF3), IRF7, and NF-?B, which translocate into the nucleus and transactivate the expression of type I and III IFNs as well as pro-inflammatory cytokines. Type I and III IFNs have overlapping functions, and both signal through the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway to induce the expression of hundreds of interferon-stimulated genes (ISGs), many of which are antiviral. The ISGs collaboratively inhibit viral proliferation and mediate viral clearance.
IFN-mediated immunity is elaborately regulated and calibrated, depending on different factors, hosts, pathogens, and environmental factors, to avoid immoderate or aberrant responses. On the other hand, however, viruses have evolved multiple strategies to evade or antagonize the antiviral immunity for survival and proliferation by interfering with the IFN induction or preventing the IFN-activated JAK-STAT signaling pathway. Dysregulation of the IFN induction and JAK-STAT signaling results in immunodeficiency and immune-mediated disorders.
This Research Topic welcomes Original Research, Review, Mini-Review and Perspective articles that cover, but are not limited to, the following topics:
• The latest discoveries in IFN-mediated antiviral immunity and some other antiviral immune response
• The modulation of innate immunity during viral infections
• Various viral evasion strategies against the innate immune response including both IFN induction and JAK-STAT signaling
As the first line of host defense against invading pathogens, the innate immune response is crucial to protect the host from viral infections. Interferons (IFNs) have been shown to be the most important defenders of innate immune system. There are three types of IFNs. Type I IFNs include IFN-a, IFN-ß, and a few other subtypes, and are produced by most cell types. Type II IFN includes only IFN-?, whose production is restricted to activated T cells, natural killer cells, and macrophages. Type III IFNs comprise IFN-?1, IFN-?2, IFN-?3, and IFN-?4, which are mainly produced by epithelial cells and dendritic cells. Host pattern recognition receptors (PRRs), including Toll-like receptors (TLRs) and RIG (retinoic-acid-inducible gene)-I-like receptors (RLRs), recognize specific pathogen-associated molecular patterns (PAMPs), which are generally viral RNA or DNA. Activation of TLR and RLR signaling pathways leads to activation of interferon regulatory factor 3 (IRF3), IRF7, and NF-?B, which translocate into the nucleus and transactivate the expression of type I and III IFNs as well as pro-inflammatory cytokines. Type I and III IFNs have overlapping functions, and both signal through the Janus kinase (JAK)–signal transducer and activator of transcription (STAT) pathway to induce the expression of hundreds of interferon-stimulated genes (ISGs), many of which are antiviral. The ISGs collaboratively inhibit viral proliferation and mediate viral clearance.
IFN-mediated immunity is elaborately regulated and calibrated, depending on different factors, hosts, pathogens, and environmental factors, to avoid immoderate or aberrant responses. On the other hand, however, viruses have evolved multiple strategies to evade or antagonize the antiviral immunity for survival and proliferation by interfering with the IFN induction or preventing the IFN-activated JAK-STAT signaling pathway. Dysregulation of the IFN induction and JAK-STAT signaling results in immunodeficiency and immune-mediated disorders.
This Research Topic welcomes Original Research, Review, Mini-Review and Perspective articles that cover, but are not limited to, the following topics:
• The latest discoveries in IFN-mediated antiviral immunity and some other antiviral immune response
• The modulation of innate immunity during viral infections
• Various viral evasion strategies against the innate immune response including both IFN induction and JAK-STAT signaling