ArticleCell host & microbe2016
STING Requires the Adaptor TRIF to Trigger Innate Immune Responses to Microbial Infection.
Article in Cell host & microbe, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 49 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
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
49 citing papers in PubMed, 84 citations in OpenAlex.
- Host Genetic Susceptibility and Antiviral Immunity Shape the Pathogenesis and Outcomes of Herpes Simplex Encephalitis.Biology · 2026Review
- Review
- Targeting the cGAS-STING pathway alleviates neuroinflammation and cognitive impairment induced by chronic infection of Toxoplasma gondii.Journal of neuroinflammation · 2026Article
- Variation in antiviral immunity and inflammation pathways precedes HIV-1 infection in a high-risk African cohort.The Journal of clinical investigation · 2026Article
- The STING Signaling: A Novel Target for Central Nervous System Diseases.Cellular and molecular neurobiology · 2025Review
- Cyclic GMP-AMP synthase recognizes the physical features of DNA.Acta pharmacologica Sinica · 2025Review
- Structural basis for TIR domain-mediated innate immune signaling by Toll-like receptor adaptors TRIF and TRAM.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- ZC3HAV1 facilitates STING activation and enhances inflammation.Communications biology · 2024Article
- The Role of cGAS-STING Signalling in Metabolic Diseases: from Signalling Networks to Targeted Intervention.International journal of biological sciences · 2024Review
- Unexpected Need of the Epidermal Growth Factor Receptor Tyrosine Kinase Activity for Signaling by Intracellular Pattern Recognition Receptors of Nucleic Acids.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023Review
- STAT2 hinders STING intracellular trafficking and reshapes its activation in response to DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Function and regulation of cGAS-STING signaling in infectious diseases.Frontiers in immunology · 2023Review
- Multifaceted functions of STING in human health and disease: from molecular mechanism to targeted strategy.Signal transduction and targeted therapy · 2022Review
- Review
- YAP inhibits HCMV replication by impairing STING-mediated nuclear transport of the viral genome.PLoS pathogens · 2022Article
- Mechanisms of TNF-independent RIPK3-mediated cell death.The Biochemical journal · 2022Review
- Comprehensive Analysis of Proteasomal Complexes in Mouse Brain Regions Detects ENO2 as a Potential Partner of the Proteasome in the Striatum.Cellular and molecular neurobiology · 2022Article
- Hyaluronic Acid Oligosaccharide Derivatives Alleviate Lipopolysaccharide-Induced Inflammation in ATDC5 Cells by Multiple Mechanisms.Molecules (Basel, Switzerland) · 2022Article
- Natterin-Induced Neutrophilia Is Dependent on cGAS/STING Activation via Type I IFN Signaling Pathway.International journal of molecular sciences · 2022Article
- Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The intracellular microbial nucleic acid sensors, TLR3 and STING, recognize pathogen molecules and signal to activate the interferon pathway. The TIR-domain containing protein TRIF is the sole adaptor of TLR3. Here, we report an essential role for TRIF in STING signaling: various activators of STING could not induce genes in the absence of TRIF. TRIF and STING interacted directly, through their carboxy-terminal domains, to promote STING dimerization, intermembrane translocation, and signaling. Herpes simplex virus (HSV), which triggers the STING signaling pathway and is controlled by it, replicated more efficiently in the absence of TRIF, and HSV-infected TRIF(-/-) mice displayed pronounced pathology. Our results indicate that defective STING signaling may be responsible for the observed genetic association between TRIF mutations and herpes simplex encephalitis in patients.
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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.