Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 51, Issue 5, Pages 1039-1061Publisher
WILEY
DOI: 10.1002/eji.202048793
Keywords
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Funding
- CSL Behring Chair of Primary Immunodeficiencies
- KU Leuven C1 Grant [C16/18/007]
- VIB GC PID Grant
- FWO [G0C8517N, G0B5120N, G0E8420N]
- Jeffrey Modell Foundation
- ERN-RITA
- Howard Hughes Medical Institute
- Rockefeller University
- St. Giles Foundation
- National Institutes of Health (NIH) [R01AI088364, R01AI127564, R01AI143810, R01NS072381, R21AI137371, R21AI151663, R37AI095983]
- National Center for Advancing Translational Sciences (NCATS), NIH Clinical and Translational Science Award (CTSA) program [UL1TR001866]
- Yale Center for Mendelian Genomics
- National Human Genome Research Institute (NHGRI) [UM1HG006504, U24HG008956]
- French National Research Agency (ANR) [ANR-10-IAHU01, ANR-18-CE93-0008-01]
- Integrative Biology of Emerging Infectious Diseases Laboratory of Excellence [ANR-10-LABX-62IBEID]
- French Foundation for Medical Research (FRM) [EQU201903007798]
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- University of Paris
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The study reveals a greater redundancy of human type I interferons for protective immunity to viruses in natural conditions than initially anticipated, while mouse type I interferons are essential for protection against a broad range of viruses in experimental settings. Various type I interferon-independent mechanisms of human cell-intrinsic immunity to viruses have yet to be discovered.
Type I IFNs are so-named because they interfere with viral infection in vertebrate cells. The study of cellular responses to type I IFNs led to the discovery of the JAK-STAT signaling pathway, which also governs the response to other cytokine families. We review here the outcome of viral infections in mice and humans with engineered and inborn deficiencies, respectively, of (i) IFNAR1 or IFNAR2, selectively disrupting responses to type I IFNs, (ii) STAT1, STAT2, and IRF9, also impairing cellular responses to type II (for STAT1) and/or III (for STAT1, STAT2, IRF9) IFNs, and (iii) JAK1 and TYK2, also impairing cellular responses to cytokines other than IFNs. A picture is emerging of greater redundancy of human type I IFNs for protective immunity to viruses in natural conditions than was initially anticipated. Mouse type I IFNs are essential for protection against a broad range of viruses in experimental conditions. These findings suggest that various type I IFN-independent mechanisms of human cell-intrinsic immunity to viruses have yet to be discovered.
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