Abstract
Interferons (IFNs) were discovered over a half-century ago as antiviral factors. The role of type I IFNs has been studied in the pathogenesis of both acute and chronic microbial infections. Deregulated type I IFN production results in a damaging cascade of cell death, inflammation, and immunological host responses that can lead to tissue injury and disease progression. Here, we summarize the role of type I IFNs in the regulation of cell death and disease during different microbial infections, ranging from viruses and bacteria to fungal pathogens. Understanding the specific mechanisms driving type I IFN-mediated cell death and disease could aid in the development of targeted therapies.
Highlights
Interferons (IFNs) are broadly classified into three groups, which are denoted as type I, II, and III based on the specific receptor utilization for their signal transduction
All of the type I IFNs bind to a common heterodimeric receptor, called the IFNα/β receptor (IFNAR), composed of two chains, IFNAR1 and IFNAR2, that are associated with the tyrosine kinases Tyk2 and Jak1
RIG-I was reported to induce type I IFN through a MAVS/TRIM25/RNF135 signaling axis following influenza infection, and was shown to have profound effects on NLRP3 inflammasome activation and IL1β secretion in human lung epithelial cells (Pothlichet et al, 2013)
Summary
Role of type I interferons in inflammasome activation, cell death, and disease during microbial infection. The Ohio State University, USA Dario S. Interferons (IFNs) were discovered over a half-century ago as antiviral factors. The role of type I IFNs has been studied in the pathogenesis of both acute and chronic microbial infections. Deregulated type I IFN production results in a damaging cascade of cell death, inflammation, and immunological host responses that can lead to tissue injury and disease progression. We summarize the role of type I IFNs in the regulation of cell death and disease during different microbial infections, ranging from viruses and bacteria to fungal pathogens. Understanding the specific mechanisms driving type I IFN-mediated cell death and disease could aid in the development of targeted therapies
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