RIPK1 Distinctly Regulates Yersinia-Induced Inflammatory Cell Death, PANoptosis
Open accessAbstract
Bacterial pathogens from the genus Yersinia cause fatal sepsis and gastritis in humans. Innate immune signaling and inflammatory cell death (pyroptosis, apoptosis, and necroptosis [PANoptosis]) serve as a first line of antimicrobial host defense. The receptor-interacting protein kinase 1 (RIPK1) is essential for Yersinia-induced pyroptosis and apoptosis and an effective host response. However, it is not clear whether RIPK1 assembles a multifaceted cell death complex capable of regulating caspase-dependent pyroptosis and apoptosis or whether there is cross-talk with necroptosis under these conditions. In this study, we report that Yersinia activates PANoptosis, as evidenced by the concerted activation of proteins involved in PANoptosis. Genetic deletion of RIPK1 abrogated the Yersinia-induced activation of the inflammasome/pyroptosis and apoptosis but enhanced necroptosis. We also found that Yersinia induced assembly of a RIPK1 PANoptosome complex capable of regulating all three branches of PANoptosis. Overall, our results demonstrate a role for the RIPK1 PANoptosome in Yersinia-induced inflammatory cell death and host defense.
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Cytokines or PAMPs trigger the assembly of a multiprotein complex called the PANoptosome.
“Cytokines or PAMPs trigger the assembly of a multiprotein complex called the PANoptosome.”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [273]
The Results section, “Yersinia induces assembly of the RIPK1 PANoptosome complex” (page unavailable), shows that Yersinia infection induces assembly of a complex containing RIPK1 and several other proteins. The Introduction describes the PANoptosome as a molecular scaffold, but the paper does not establish that cytokines or isolated PAMPs trigger its assembly. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe PANoptosome includes various molecules necessary for the activation of downstream programmed cell death (PCD) effectors such as GSDMD, GSDME, CASP3/7, and MLKL.
“This complex includes various molecules necessary for the activation of downstream programmed cell death (PCD) effectors such as GSDMD, GSDME, CASP3/7, and MLKL (Fig. 4).”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [273]
The Introduction (page unavailable) describes the PANoptosome as a scaffold engaging molecules from pyroptosis, apoptosis, and necroptosis. The Results sections on PANoptosome assembly and Yersinia-induced PANoptosis (pages unavailable) identify complex components and report activation of GSDMD, CASP3/7, and MLKL-associated signaling. Our copy does not identify GSDME as a downstream effector in this context. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPANoptosis is a united modality of inflammatory programmed cell death, accompanied by markers of apoptosis, necrosis, and pyroptosis pathways.
“PANoptosis, is a united modality of inflammatory programmed cell death, accompanied by markers of apoptosis, necrosis, and pyroptosis pathways.271–275”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [273]
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References 56 · Cited by 224
- Authors
- Malireddi, R. K. S., Kesavardhana, S., Karki, R., Kancharana, B., Burton, A. R., & Kanneganti, T.-D.
- Affiliations
- St. Jude Children's Research Hospital (US)
- Corresponding author
- Kanneganti, Thirumala-Devi
- ORCID
- Venue
- ImmunoHorizons
- Publisher
- Oxford University Press (OUP)
- Published
- 2020-12-01
- Volume
- 4
- Issue
- 12
- Pages
- 789-796
- ISSN
- 2573-7732 (ISSN-L)
- PMC
- PMC7906112
- OpenAlex
- W3110985405
- Cited by
- 224
- References
- 56
- Citations by year
- 2026: 53 · 2025: 57 · 2024: 53 · 2023: 33 · 2022: 17 · 2021: 11
- FWCI
- 4.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- ImmunoHorizons (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Seoul National University Open Repository (Seoul National University) (submittedVersion)
- Funders
- American Lebanese Syrian Associated Charities (AI124346, AR056296, AI101935)
- National Institutes of Health (AI 101935)
- National Cancer Institute (R35CA253095)
- National Institute of Allergy and Infectious Diseases (R01AI101935, R37AI101935, R01AI124346)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR056296)
- Topics
- 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
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- RIPK1, PANoptosis, Yersinia, pyroptosis, apoptosis, necroptosis, PANoptosome, inflammasome, inflammatory cell death, innate immunity, host defense, bacterial sepsis
- MeSH terms
- Pyroptosis, Necroptosis, Animals, Inflammation, Macrophages, Mice, Inbred C57BL, Yersinia pseudotuberculosis, Signal Transduction, Mice, Receptor-Interacting Protein Serine-Threonine Kinases, Inflammasomes
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