ArticleCell reports2018
Detrimental Type I Interferon Signaling Dominates Protective AIM2 Inflammasome Responses during Francisella novicida Infection.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.Frontiers in immunology · 2026Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- The role of pyroptosis in ovarian cancer.Discover oncology · 2025Review
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- PANoptosis in Bacterial Infections: A Double-Edged Sword Balancing Host Immunity and Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Inflammasomes: potential therapeutic targets in hematopoietic stem cell transplantation.Cell communication and signaling : CCS · 2024Review
- The Generation of Genetically Engineered Human Induced Pluripotent Stem Cells Overexpressing IFN-β for Future Experimental and Clinically Oriented Studies.International journal of molecular sciences · 2024Article
- Insights into ubiquitinome dynamics in the host‒pathogen interplay during Francisella novicida infection.Cell communication and signaling : CCS · 2024Article
- Role of Type I Interferons duringBiomolecules · 2024Review
- The multiple faces of cGAS-STING in antitumor immunity: prospects and challenges.Medical review (2021) · 2024Review
- SAM68 directs STING signaling to apoptosis in macrophages.Communications biology · 2024Article
- Article
- Pyroptosis: the dawn of a new era in endometrial cancer treatment.Frontiers in oncology · 2023Review
- Pathogen-selective killing by guanylate-binding proteins as a molecular mechanism leading to inflammasome signaling.Nature communications · 2022Article
- Review
- Intracranial delivery of synthetic mRNA to suppress glioblastoma.Molecular therapy oncolytics · 2022Article
- Inhibition of the cGAS-STING Pathway Attenuates Lung Ischemia/Reperfusion Injury via Regulating Endoplasmic Reticulum Stress in Alveolar Epithelial Type II Cells of Rats.Journal of inflammation research · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Interferons (IFNs) and inflammasomes are essential mediators of anti-microbial immunity. Type I IFN signaling drives activation of the AIM2 inflammasome in macrophages; however, the relative contribution of IFNs and inflammasome responses in host defense is less understood. We report intact AIM2 inflammasome responses in mice lacking type I IFN signaling during infection with F. novicida. Lack of type I IFN signaling conferred protection to F. novicida infection in contrast to the increased susceptibility in AIM2-deficient mice. Mice lacking both AIM2 and IFNAR2 were protected against the infection. The detrimental effects of type I IFN signaling were due to its ability to induce activation of apoptotic caspases and cell death. These results demonstrate the contrasting effects of type I IFN signaling and AIM2 during F. novicida infection in vivo and indicate a dominant role for type I IFNs in mediating detrimental responses despite the protective AIM2 inflammasome responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.