ArticleCell reports2016
Type I Interferon Induction by Neisseria gonorrhoeae: Dual Requirement of Cyclic GMP-AMP Synthase and Toll-like Receptor 4.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
- Interferon-epsilon, an estrogen-induced type I interferon, is uniquely exploited by Neisseria gonorrhoeae via effects on sialic acid metabolism.Cell host & microbe · 2025Article
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- Extracellular vesicles from diverse fungal pathogens induce species-specific and endocytosis-dependent immunomodulation.PLoS pathogens · 2025Article
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- Review
- A Cancer Nanovaccine for Co-Delivery of Peptide Neoantigens and Optimized Combinations of STING and TLR4 Agonists.ACS nano · 2024Article
- Airway epithelial cGAS inhibits LPS-induced acute lung injury through CREB signaling.Cell death & disease · 2023Article
- Immunomodulatory Role of Interferons in Viral and Bacterial Infections.International journal of molecular sciences · 2023Review
- RNF5: inhibiting antiviral immunity and shaping virus life cycle.Frontiers in immunology · 2023Review
- Mechanisms of host manipulation byFrontiers in microbiology · 2023Review
- Neisseria gonorrhoeae Infection in Women Increases With Rising Gonococcal Burdens in Partners: Chlamydia Coinfection in Women Increases Gonococcal Burden.The Journal of infectious diseases · 2022Article
- Article
- Post-Translational Modifications of cGAS-STING: A Critical Switch for Immune Regulation.Cells · 2022Review
- The multifaceted functions of cGAS.Journal of molecular cell biology · 2022Review
- Signaling pathways in obesity: mechanisms and therapeutic interventions.Signal transduction and targeted therapy · 2022Review
- Control of innate immunity by the cGAS-STING pathway.Immunology and cell biology · 2022Review
- Article
- cGAS exacerbates Schistosoma japonicum infection in a STING-type I IFN-dependent and independent manner.PLoS pathogens · 2022Article
- A Variety of Nucleic Acid Species Are Sensed by cGAS, Implications for Its Diverse Functions.Frontiers in immunology · 2022Review
- The cGAS-STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy.Acta pharmaceutica Sinica. B · 2022Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
The innate immune system is the first line of defense against Neisseria gonorrhoeae (GC). Exposure of cells to GC lipooligosaccharides induces a strong immune response, leading to type I interferon (IFN) production via TLR4/MD-2. In addition to living freely in the extracellular space, GC can invade the cytoplasm to evade detection and elimination. Double-stranded DNA introduced into the cytosol binds and activates the enzyme cyclic-GMP-AMP synthase (cGAS), which produces 2'3'-cGAMP and triggers STING/TBK-1/IRF3 activation, resulting in type I IFN expression. Here, we reveal a cytosolic response to GC DNA that also contributes to type I IFN induction. We demonstrate that complete IFN-β induction by live GC depends on both cGAS and TLR4. Type I IFN is detrimental to the host, and dysregulation of iron homeostasis genes may explain lower bacteria survival in cGAS(-/-) and TLR4(-/-) cells. Collectively, these observations reveal cooperation between TLRs and cGAS in immunity to GC infection.
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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.