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Apoptotic Caspases Suppress mtDNA-Induced STING-Mediated Type I IFN Production
Open accessAbstract
Activated caspases are a hallmark of apoptosis induced by the intrinsic pathway, but they are dispensable for cell death and the apoptotic clearance of cells in vivo. This has led to the suggestion that caspases are activated not just to kill but to prevent dying cells from triggering a host immune response. Here, we show that the caspase cascade suppresses type I interferon (IFN) production by cells undergoing Bak/Bax-mediated apoptosis. Bak and Bax trigger the release of mitochondrial DNA. This is recognized by the cGAS/STING-dependent DNA sensing pathway, which initiates IFN production. Activated caspases attenuate this response. Pharmacological caspase inhibition or genetic deletion of caspase-9, Apaf-1, or caspase-3/7 causes dying cells to secrete IFN-β. In vivo, this precipitates an elevation in IFN-β levels and consequent hematopoietic stem cell dysfunction, which is corrected by loss of Bak and Bax. Thus, the apoptotic caspase cascade functions to render mitochondrial apoptosis immunologically silent.
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“In the absence of active caspases, mtDNA released following mitochondrial outer membrane permeabilization triggers type I interferon responses in a cGAS–STING-dependent manner143,144”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [144]
Experimental — accuracy not yet measuredIn the citing paper
“These include: (1) the prominent ability of CASP8 to inhibit necroptosis (see above), which is generally associated with the establishment of robust inflammatory responses linked to NF-κB activation [496 925–928]; (2) the capacity of CASP3 to drive PS exposure (see above), which generally supports the phagocytic removal of dying and dead cells while delivering anti-inflammatory signals to”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [932]
In the citing paper
“MtDNA has been reported to activate immunity through two distinct pathways, namely Toll-like receptor 9 (TLR9; Zhang et al, 2010;Oka et al, 2012;Liu et al, 2015), and cGAS activation (White et al, 2014;West et al, 2015).”
From Mitochondrial DNA and TLR9 drive muscle inflammation upon Opa1 deficiency (2018) · cites this paper as White et al, 2014
In the citing paper
“Thus, cytosolic mtDNA activates the DNA sensor cGAS and promotes STING-IRF3-dependent signaling (Rongvaux et al, 2014;White et al, 2014;West et al, 2015).”
From Mitochondrial DNA and TLR9 drive muscle inflammation upon Opa1 deficiency (2018) · cites this paper as White et al, 2014
In the citing paper
“Interestingly, these events were attenuated by caloric restriction (White et al., 2014), an intervention which has been shown to extend lifespan in a plethora of organisms and decrease the burden of senescent cells (Fontana et al., 2018; Mercken et al., 2012).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as White et al., 2014
In the citing paper
“Finally, ABT-737 (an experimental inhibitor of multiple BCL2 family members) is known for its ability to drive robust type I IFN secretion by cancer cells downstream of mtDNA-driven CGAS activation, especially in the context of caspases inhibition (Rongvaux et al., 2014; White et al., 2014).”
From Immunomodulation by targeted anticancer agents (2021) · cites this paper as White et al., 2014
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“fmk, and cycloheximide causes Bak/Bax-dependent mitochondrial damage (Irrinki et al., 2011) and that Bak / Bax / MEFs are partially protected from necroptotic death induced by TNFa, Q-VD-Oph, and a Smac mimetic (TSQ) (Moujalled et al.”
Nonomura, K., Yamaguchi, Y., Hamachi, M., Koike, M., Uchiyama, Y., Nakazato, K., Mochizuki, A., Sakaue-Sawano, A., Miyawaki, A., Yoshida, H., et al. (2013) · Developmental Cell · doi:10.1016/j.devcel.2013.11.015 · Cited by 103 · cited 1×
“In the brain, controversy exists as to the extent of cell death in mice lacking the caspase cascade, and recent studies indicate that changes in morphogen gradients may underpin aberrant forebrain development (Honarpour et al., 2001; Nonomura et al., 2013; Oppenheim et al., 2001).”
Apoptosis and non-inflammatory phagocytosis can be induced by mitochondrial damage without caspases
van Delft, M. F., Smith, D. P., Lahoud, M. H., Huang, D. C. S., & Adams, J. M. (2009) · Cell Death and Differentiation · doi:10.1038/cdd.2009.166 · Cited by 50
Self-citationType I Interferons as Ambiguous Modulators of Chronic Inflammation in the Central Nervous System
Prinz, M., & Knobeloch, K. (2012) · Frontiers in Immunology · doi:10.3389/fimmu.2012.00067 · Cited by 36
Labi, V., Bertele, D., Woess, C., Tischner, D., Bock, F. J., Schwemmers, S., Pahl, H. L., Geley, S., Kunze, M., Niemeyer, C. M., et al. (2012) · EMBO Molecular Medicine · doi:10.1002/emmm.201201235 · Cited by 32 · cited 1×
“Similar effects have been reported for HSCs lacking Bim (Labi et al., 2013).”
Bcl-2 expression and apoptosis in the regulation of hematopoietic stem cells
Orelio, C. C., & Dzierzak, E. A. (2007) · Leukemia & lymphoma/Leukemia and lymphoma · doi:10.1080/10428190601032529 · Cited by 20 · cited 1×
“This has led to a model whereby a proportion of HSCs undergo apoptosis during the normal course of hematopoiesis; hence, a reduction in apoptosis is proposed to lead to accumulation of HSCs in vivo (Orelio and Dzierzak, 2007).”
Honarpour, N., Tabuchi, K., Stark, J. M., Hammer, R. E., Südhof, T. C., Parada, L. F., Wang, X., Richardson, J. A., & Herz, J. (2001) · Neuroscience · doi:10.1016/s0306-4522(01)00275-5 · Cited by 20 · cited 1×
“In the brain, controversy exists as to the extent of cell death in mice lacking the caspase cascade, and recent studies indicate that changes in morphogen gradients may underpin aberrant forebrain development (Honarpour et al., 2001; Nonomura et al., 2013; Oppenheim et al., 2001).”
O'Brien, T., & Dixit, V. M. (2009) · Encyclopedia of Life Sciences · doi:10.1002/9780470015902.a0021587 · Cited by 2 · cited 1×
“They include the caspase-1 inhibitors VX-740 and VX-765 (Belnacasan) and the pan-caspase inhibitors IDN-6556 (Emricasan) and GS-9450 (O’Brien and Dixit, 2009).”
Cited by
Sorted by citations
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680
“Of note, lysosome-dependent cell death does not necessarily involve MOMP and caspases, and does not necessarily manifest with an apoptotic morphotype [782].”
BackgroundInfluentialTargeting apoptosis in cancer therapy
Carneiro, B. A., & El‐Deiry, W. S. (2020) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-020-0341-y · Cited by 2,676
Mitochondria as multifaceted regulators of cell death
Bock, F. J., & Tait, S. W. G. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0173-8 · Cited by 2,531
The cGAS–STING pathway as a therapeutic target in inflammatory diseases
Decout, A., Katz, J. D., Venkatraman, S., & Ablasser, A. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-021-00524-z · Cited by 2,309
Regulation of apoptosis in health and disease: the balancing act of BCL-2 family proteins
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Metadata
- Authors
- White, M. J., McArthur, K., Metcalf, D., Lane, R. M., Cambier, J. C., Herold, M. J., van Delft, M. F., Bedoui, S., Lessene, G., Ritchie, M. E., Huang, D. C. S., & Kile, B. T.
- Affiliations
- The University of Melbourne (AU)
- Walter and Eliza Hall Institute of Medical Research (AU)
- National Jewish Health (US)
- Corresponding author
- White, Michael J.
- Kile, Benjamin T.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-12
- Volume
- 159
- Issue
- 7
- Pages
- 1549-1562
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4520319
- OpenAlex
- W2028107828
- Cited by
- 983
- References
- 68
- Citations by year
- 2026: 89 · 2025: 88 · 2024: 118 · 2023: 107 · 2022: 111 · 2021: 94 · 2020: 93 · 2019: 61 · 2018: 76 · 2017: 63 · 2016: 39 · 2015: 40
- FWCI
- 21.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R21AI099346)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- caspases, apoptosis, type I interferon, STING, cGAS, mitochondrial DNA, Bak, Bax, caspase-9, Apaf-1, caspase-3, caspase-7, interferon-beta, hematopoietic stem cells
- MeSH terms
- STING Protein, Animals, Crosses, Genetic, DNA, Mitochondrial, Female, Hematopoietic Stem Cells, Interferon Type I, Male, Membrane Proteins, Mice, Inbred C57BL, Signal Transduction, Apoptosis, Caspases, Caspase 9
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