Interleukin-1β Induces mtDNA Release to Activate Innate Immune Signaling via cGAS-STING
Open accessAbstract
Interleukin-1 beta (IL-1β) is a pleiotropic mediator of inflammation and is produced in response to a wide range of stimuli. During infection, IL-1β production occurs in parallel with the onset of innate antimicrobial defenses, but the contribution of IL-1β signaling to cell-intrinsic immunity is not defined. Here, we report that exogenous IL-1β induces interferon regulatory factor 3 (IRF3) activation in human myeloid, fibroblast, and epithelial cells. IRF3 activation by IL-1β is dependent upon the DNA-sensing pathway adaptor, stimulator of interferon genes (STING), through the recognition of cytosolic mtDNA by cyclic guanosine monophosphate (GMP)-AMP synthase (cGAS). IL-1β treatment results in interferon (IFN) production and activation of IFN signaling to direct a potent innate immune response that restricts dengue virus infection. This study identifies a new function for IL-1β in the onset or enhancement of cell-intrinsic immunity, with important implications for cGAS-STING in integrating inflammatory and microbial cues for host defense.
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Mitochondrial DNA or mitochondrial RNA released into the cytosol through BAX-BAK macropores can activate cytosolic nucleic acid sensors independently of cell death, leading to type I interferon production.
“mtDNA or mtRNA released into the cytosol via BAX–BAK macropores can activate nucleic acid sensors in the cytosol145 independently of cell death130,146,147, ultimately leading to the production of type I interferon”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [146]
The Results and Discussion report that IL-1β induces cytosolic mtDNA release without detectable cell death, followed by cGAS–STING signaling and IFNB1 induction (pages not provided). The paper does not establish release through BAX–BAK macropores or show that mtRNA drives this response; its Discussion says the mechanism of mtDNA release remains unknown. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIL-1β, a major SASP factor, can induce mtDNA release with subsequent activation of pro-inflammatory pathways.
“IL-1β, a major SASP factor, can induce mtDNA release with subsequent activation of pro-inflammatory pathways (Aarreberg et al., 2019).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Aarreberg et al., 2019
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- Authors
- Aarreberg, L. D., Esser-Nobis, K., Driscoll, C., Shuvarikov, A., Roby, J. A., & Gale, M.
- Affiliations
- University of Washington (US)
- Corresponding author
- Gale, Michael
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2019-05
- Volume
- 74
- Issue
- 4
- Pages
- 801-815.e6
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC6596306
- OpenAlex
- W2934093192
- Cited by
- 328
- References
- 58
- Citations by year
- 2026: 39 · 2025: 37 · 2024: 65 · 2023: 60 · 2022: 41 · 2021: 47 · 2020: 31 · 2019: 8
- FWCI
- 12.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Charles Sturt University Research Output (CRO) (submittedVersion, cc-by-nc-nd)
- Funders
- NIH (AI27463, AI118916, AI100625, AI104002, AI083019, T32AI106677-03)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- IL-1β, mitochondrial DNA release, cGAS-STING pathway, IRF3 activation, interferon signaling, innate immunity, dengue virus, cell-intrinsic immunity, DNA sensing, infection and inflammation
- MeSH terms
- STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Dengue, Dengue Virus, DNA, Mitochondrial, Cyclic GMP, Humans, Immunity, Innate, Inflammation, Interferons, Membrane Proteins, Nucleotidyltransferases, Signal Transduction, Myeloid Cells, Interferon Regulatory Factor-3, Interleukin-1beta, Host-Pathogen Interactions
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