ArticleFrontiers in immunology2022
Activation of the AIM2 Receptor in Circulating Cells of Post-COVID-19 Patients With Signs of Lung Fibrosis Is Associated With the Release of IL-1α, IFN-α and TGF-β.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Pooled it
- Targeting pyroptosis in myocardial inflammation and fibrosis: molecular mechanisms and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2025Review
- Do Long COVID and COVID Vaccine Side Effects Share Pathophysiological Picture and Biochemical Pathways?International journal of molecular sciences · 2025Review
- Integrated proteomics highlights functional activation induced by advanced-platelet rich fibrin plus (A-PRF +) in primary equine fibroblasts.Scientific reports · 2025Article
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Review
- Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.Biomedicines · 2025Review
- Conventional Chemotherapy and Inflammation: What Is the Role of the Inflammasome in the Tumor Microenvironment?Biomedicines · 2025Review
- Review
- Association between COVID-19 Severity and Expression of Viral Nucleic Acid Sensor Genes in Peripheral Blood Mononuclear Cells and Nasopharyngeal Epithelial Cells.The American journal of tropical medicine and hygiene · 2024Article
- Mechanisms of long COVID: An updated review.Chinese medical journal pulmonary and critical care medicine · 2023Review
- Review
- Inflammasomes during SARS-CoV-2 infection and development of their corresponding inhibitors.Frontiers in cellular and infection microbiology · 2023Review
- Cytoplasmic DNAs: Sources, sensing, and roles in the development of lung inflammatory diseases and cancer.Frontiers in immunology · 2023Review
- Microvascular significance of TGF-β axis activation in COVID-19.Frontiers in cardiovascular medicine · 2022Review
- Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), responsible for COVID-19, has caused a global pandemic. Observational studies revealed a condition, herein called as Long-COVID syndrome (PC), that affects both moderately and severely infected patients, reducing quality-of-life. The mechanism/s underlying the onset of fibrotic-like changes in PC are still not well defined. The goal of this study was to understand the involvement of the Absent in melanoma-2 (AIM2) inflammasome in PC-associated lung fibrosis-like changes revealed by chest CT scans. Peripheral blood mononuclear cells (PBMCs) obtained from PC patients who did not develop signs of lung fibrosis were not responsive to AIM2 activation by Poly dA:dT. In sharp contrast, PBMCs from PC patients with signs of lung fibrosis were highly responsive to AIM2 activation, which induced the release of IL-1α, IFN-α and TGF-β. The recognition of Poly dA:dT was not due to the activation of cyclic GMP-AMP (cGAMP) synthase, a stimulator of interferon response (cGAS-STING) pathways, implying a role for AIM2 in PC conditions. The release of IFN-α was caspase-1- and caspase-4-dependent when AIM2 was triggered. Instead, the release of pro-inflammatory IL-1α and pro-fibrogenic TGF-β were inflammasome independent because the inhibition of caspase-1 and caspase-4 did not alter the levels of the two cytokines. Moreover, the responsiveness of AIM2 correlated with higher expression of the receptor in circulating CD14+ cells in PBMCs from patients with signs of lung fibrosis.
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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 Socratic graph.