ArticleiScience2022
The STING1-MYD88 complex drives ACOD1/IRG1 expression and function in lethal innate immunity.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Itaconate metabolism in regulated cell death.Molecular and cellular biochemistry · 2026Review
- The alkylation of AIM2 by itaconate mediates macrophage PANoptosis during sepsis.Cellular & molecular immunology · 2026Article
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- STAT1 itaconation prevents macrophage cytolistic mtDNA -induced inflammation in wear particle-induced aseptic loosening.Cell communication and signaling : CCS · 2026Article
- Itaconate modifications: Mechanisms and applications.Journal of intensive medicine · 2026Review
- Itaconate modulates myeloid inflammation in myocardial infarction via metabolic and structural reprogramming.Genes & genomics · 2026Article
- STING-mediated antiviral response: insights into MVA replication control in avian cells.Microbiology spectrum · 2025Article
- Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Orchestrating intratumoral DC-T cell immunity for enhanced tumor control via radiotherapy-activated TLR7/8 prodrugs in mice.Nature communications · 2025Article
- Pharmacological inhibition of STING-mediated GPX4 autophagic degradation by 4-octyl itaconate ameliorates sepsis-induced acute kidney injury.Apoptosis : an international journal on programmed cell death · 2025Article
- ELF4 improves sepsis-induced myocardial injury by regulating STING signaling-mediated T cells differentiation.Cell biology and toxicology · 2025Article
- A neuroimmune pathway drives bacterial infection.Science advances · 2025Article
- Article
- Zebrafish use conserved CLR and TLR signaling pathways to respond to fungal PAMPs in zymosan.Developmental and comparative immunology · 2025Article
- Dopamine as an endogenous regulator of innate immunity in sepsis.Frontiers in immunology · 2025Review
- Cancer cell-intrinsic biosynthesis of itaconate promotes tumor immunogenicity.The EMBO journal · 2024Article
- The role and therapeutic potential of itaconate in lung disease.Cellular & molecular biology letters · 2024Review
- Toward decoding spatiotemporal signaling activities of reactive immunometabolites with precision immuno-chemical biology tools.Communications chemistry · 2024Review
- Metabolic Messengers: itaconate.Nature metabolism · 2024Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ACOD1 (also known as IRG1) has emerged as a regulator of immunometabolism that operates by producing metabolite itaconate. Here, we report a key role of STING1 (also known as STING and TMEM173) in mediating ACOD1 expression in myeloid cells in response to toll-like receptor (TLR) signaling. The activation of STING1 through exogenous cyclic dinucleotides (e.g., 3'3'-cGAMP) or endogenous gain-of-function mutation (e.g., V155M) enhances lipopolysaccharide-induced ACOD1 expression and itaconate production in macrophages and monocytes, whereas the deletion of STING1 blocks this process. The adaptor protein MYD88, instead of DNA sensor cyclic GMP-AMP synthase (CGAS), favors STING1-dependent ACOD1 expression. Mechanistically, MYD88 directly blocks autophagic degradation of STING1 and causes subsequent IRF3/JUN-mediated ACOD1 gene transcription. Consequently, the conditional deletion of STING1 in myeloid cells fails to produce ACOD1 and itaconate, thereby protecting mice against endotoxemia and polymicrobial sepsis. Our results, therefore, establish a direct link between TLR4 signaling and ACOD1 expression through the STING1-MYD88 complex during septic shock.
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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 OpenQuestion graph.