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IL-1R signaling in dendritic cells replaces pattern-recognition receptors in promoting CD8(+) T cell responses to influenza A virus
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Immune responses to vaccines require direct recognition of pathogen-associated molecular patterns (PAMPs) through pattern-recognition receptors (PRRs) on dendritic cells (DCs). Unlike vaccination, infection by a live pathogen often impairs DC function and inflicts additional damage on the host. Here we found that after infection with live influenza A virus, signaling through the interleukin 1 receptor (IL-1R) was required for productive priming of CD8(+) T cells, but signaling through the PRRs TLR7 and RIG-I was not. DCs activated by IL-1 in trans were both required and sufficient for the generation of virus-specific CD8(+) T cell immunity. Our data demonstrate a critical role for a bystander cytokine in the priming of CD8(+) T cells during infection with a live virus.
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“Evidence has been provided previously that IL-1 can replace a need for PRRs in activation of DCs and promotion of CD8+ T cell responses.50”
From TLR9-independent CD8+ T cell responses in hepatic AAV gene transfer through IL-1R1-MyD88 signaling (2024) · cites this paper as [50]
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Metadata
- Authors
- Pang, I. K., Ichinohe, T., & Iwasaki, A.
- Affiliations
- Yale University (US)
- Corresponding author
- Iwasaki, Akiko
- Venue
- Nature Immunology
- Published
- 2013-01-13
- Volume
- 14
- Issue
- 3
- Pages
- 246-253
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC3577947
- OpenAlex
- W2035396878
- Cited by
- 145
- References
- 44
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 4 · 2023: 8 · 2022: 5 · 2021: 15 · 2020: 8 · 2019: 10 · 2018: 11 · 2017: 19 · 2016: 13 · 2015: 21 · 2014: 12 · 2013: 10
- FWCI
- 10.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Japan Society for the Promotion of Science (23790506)
- National Cancer Institute
- National Institute of Allergy and Infectious Diseases (R01AI062428, R56AI062428, AI062428 AND U54 AI057160, U54AI057160)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- IL-1 signaling, dendritic cells, CD8+ T cell priming, influenza A virus infection, pattern recognition receptors, TLR7, RIG-I, innate immunity
- MeSH terms
- Roundabout Proteins, Animals, Cell Differentiation, Cell Movement, Dendritic Cells, Interleukin-1, Lymphocyte Activation, Membrane Glycoproteins, Membrane Proteins, Mice, Inbred C57BL, Nerve Tissue Proteins, Orthomyxoviridae Infections, Influenza A virus, Receptors, Cell Surface, Signal Transduction, Receptors, Interleukin-1, Mice, Knockout, CD8-Positive T-Lymphocytes, Receptors, Pattern Recognition, Toll-Like Receptor 7, Mice, Myeloid Differentiation Factor 88, Receptors, CCR7
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