Journal
SEMINARS IN IMMUNOLOGY
Volume 43, Issue -, Pages -Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2019.05.001
Keywords
Interferon; Chronic virus infection; Immune response; T cell; Innate immunity; Adaptive immunity; Exhaustion; Interferon regulatory factor; IRF; Interferon stimulatory gene; IS G
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Funding
- Canadian Institutes of Health Research (CIHR) Foundation Grant [FDN148386]
- National Institutes of Health (NIH) [AI085043]
- Scotiabank Research Chair
- Helena Lam Fellowship in Cancer Research Fellowship
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Type I Interferons (IFN-I) mediate numerous immune interactions during viral infections, from the establishment of an antiviral state to invoking and regulating innate and adaptive immune cells that eliminate infection. While continuous IFN-I signaling plays critical roles in limiting virus replication during both acute and chronic infections, sustained IFN-I signaling also leads to chronic immune activation, inflammation and, consequently, immune exhaustion and dysfunction. Thus, an understanding of the balance between the desirable and deleterious effects of chronic IFN-I signaling will inform our quest for IFN-based therapies for chronic viral infections as well as other chronic diseases, including cancer. As such the factors involved in induction, propagation and regulation of IFN-I signaling, from the initial sensing of viral nucleotides within the cell to regulatory downstream signaling factors and resulting IFN-stimulated genes (ISGs) have received significant research attention. This review summarizes recent work on IFN-I signaling in chronic infections, and provides an update on therapeutic approaches being considered to counter such infections.
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