ArticleInflammation2018
AIM2 Inflammasome Is Critical for dsDNA-Induced IL-1β Secretion in Human Dental Pulp Cells.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Application of the Er:YAG laser in pulpotomy for mature permanent teeth with pulpitis: An animal study.PloS one · 2026Article
- The Role of Inflammasomes in Chronic Oral Inflammatory Disease and Oral Cancer: A Narrative Review.Dentistry journal · 2025Review
- Roles of Pyroptosis in the Progression of Pulpitis and Apical Periodontitis.Journal of inflammation research · 2025Review
- The role of AIM2 in inflammation and tumors.Frontiers in immunology · 2024Review
- AIM2 Inflammasome's First Decade of Discovery: Focus on Oral Diseases.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The AIM2 inflammasome pathway has been determined to play an important role in cellular immune defense against bacterial and viral infections; however, its function and regulatory mechanism in human dental pulp cells (HDPCs) during pulpitis remains poorly understood. In this study, we explored whether the AIM2 inflammasome pathway was activated in HDPCs in response to dsDNA and defined its role in regulating IL-1β secretion. We demonstrated that stimulation with IFN-γ and cytoplasmic DNA significantly activated the AIM2 inflammasome and increased IL-1β secretion in HDPCs. Moreover, AIM2 overexpression significantly up-regulated both cleaved Caspase-1 expression and IL-1β release in HDPCs, while suppression of ASC and Caspase-1 resulted in down-regulation of cleaved Caspase-1 and IL-1β secretion. These results suggest that Caspase-1-dependent IL-1β processing and secretion require the AIM2 inflammasome pathway in HDPCs and that the AIM2 inflammasome pathway is critical for regulation of the dental pulp immune response.
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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.