ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Aim2 deficiency stimulates the expression of IFN-inducible Ifi202, a lupus susceptibility murine gene within the Nba2 autoimmune susceptibility locus.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 80 citations in OpenAlex.
- Inflammasomes in Sjögren's Disease: Exploring the Therapeutic Value.International journal of molecular sciences · 2026Review
- Deletion of absent in melanoma-2 (AIM2) drives bone marrow adipogenesis and impairs bone microarchitecture.GeroScience · 2025Article
- DNA sensors in metabolic and cardiovascular diseases: Molecular mechanisms and therapeutic prospects.Immunological reviews · 2025Review
- cGAS-STING, inflammasomes and pyroptosis: an overview of crosstalk mechanism of activation and regulation.Cell communication and signaling : CCS · 2024Review
- The Role of the AIM2 Gene in Obesity-Related Glucose and Lipid Metabolic Disorders: A Recent Update.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Article
- Inflammasome activation by viral infection: mechanisms of activation and regulation.Frontiers in microbiology · 2023Review
- dsDNA-induced AIM2 pyroptosis halts aberrant inflammation during rhabdomyolysis-induced acute kidney injury.Cell death and differentiation · 2022Article
- Insights into inflammasome regulation: cellular, molecular, and pathogenic control of inflammasome activation.Immunologic research · 2022Review
- The complex role of AIM2 in autoimmune diseases and cancers.Immunity, inflammation and disease · 2021Review
- AIM2 in health and disease: Inflammasome and beyond.Immunological reviews · 2020Review
- Inflammasomes in the pathophysiology of autoinflammatory syndromes.Journal of leukocyte biology · 2020Review
- Deficiency in AIM2 induces inflammation and adipogenesis in white adipose tissue leading to obesity and insulin resistance.Diabetologia · 2019Article
- Type I interferon (IFN)-inducible Absent in Melanoma 2 proteins in neuroinflammation: implications for Alzheimer's disease.Journal of neuroinflammation · 2019Review
- Roles of Inflammasomes in Inflammatory Kidney Diseases.Mediators of inflammation · 2019Review
- Inhibition of AIM2 inflammasome activation by a novel transcript isoform of IFI16.EMBO reports · 2018Article
- Sex Differences in Correlation with Gene Expression Levels betweenJournal of immunology research · 2018Article
- Role of inflammasomes in inflammatory autoimmune rheumatic diseases.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Review
- Priming and Activation of Inflammasome by Canarypox Virus Vector ALVAC via the cGAS/IFI16-STING-Type I IFN Pathway and AIM2 Sensor.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Absent in Melanoma 2 proteins in SLE.Clinical immunology (Orlando, Fla.) · 2017Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Murine Aim2 and p202 proteins (encoded by the Aim2 and Ifi202 genes) are members of the IFN-inducible p200 protein family. Both proteins can sense dsDNA in the cytoplasm. However, upon sensing dsDNA, only the Aim2 protein through its pyrin domain can form an inflammasome to activate caspase-1 and induce cell death. Given that the p202 protein has been predicted to inhibit the activation of caspase-1 by the Aim2 protein and that increased levels of the p202 protein in female mice of certain strains are associated with lupus susceptibility, we compared the expression of Aim2 and Ifi202 genes between Aim2-deficient and age-matched wild-type mice. We found that the Aim2 deficiency in immune cells stimulated the expression of Ifi202 gene. The increased levels of the p202 protein in cells were associated with increases in the expression of IFN-β, STAT1, and IFN-inducible genes. Moreover, after knockdown of Aim2 expression in the murine macrophage cell line J774.A1, IFN-β treatment of cells robustly increased STAT1 protein levels (compared with those of control cells), increased the activating phosphorylation of STAT1 on Tyr-701, and stimulated the activity of an IFN-responsive reporter. Notably, the expression of Aim2 in non-lupus-prone (C57BL/6 and B6.Nba2-C) and lupus-prone (B6.Nba2-ABC) splenic cells and in a murine macrophage cell line that overexpressed p202 protein was found to be inversely correlated with Ifi202. Collectively, our observations demonstrate an inverse correlation between Aim2 and p202 expressions. We predict that defects in Aim2 expression within immune cells contribute to increased susceptibility to lupus.
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