ArticleThe Journal of clinical investigation2010
NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 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
142 citing papers in PubMed, 252 citations in OpenAlex.
- Possible Involvement of the Mucosal Claudin Expression in the Healing of a Refractory Ileocecal Ulcer in a Patient with Crohn's Disease Successfully Treated with Infliximab.Internal medicine (Tokyo, Japan) · 2026Article
- Tumour-Derived Extracellular Vesicles Reprogramme Tumour-Associated Macrophages Into Immunosuppressive Phenotype via NOD1 Signalling in Clear Cell Renal Cell Carcinoma.Journal of extracellular vesicles · 2026Article
- Role of Nod-like Receptors inMicroorganisms · 2026Review
- Article
- Filamentous bacteriophages: impact on prokaryotic virulence, eukaryotic immunity, and implications for phage therapy.Frontiers in immunology · 2026Review
- Interferons in health and disease.Cell · 2025Review
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- Type 1 interferon signature and allograft inflammatory factor-1 contribute to refractoriness to TNF inhibition in ankylosing spondylitis.Nature communications · 2025Article
- The immune system in cardiovascular diseases: from basic mechanisms to therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Filamentous bacteriophage M13 induces proinflammatory responses in intestinal epithelial cells.Infection and immunity · 2025Article
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- Vitamin A deficiency enhances susceptibility to experimental autoimmune pancreatitis through activation of CD4+ T cells expressing CXCR3 and secreting CCL25.Clinical and experimental immunology · 2025Article
- Advances in modeling gastric intestinal metaplasia: a comprehensive review of experimental models and mechanistic insights.Frontiers in oncology · 2025Review
- Pattern Recognition by NOD-Like Receptors.Advances in experimental medicine and biology · 2025Review
- RIG-I drives protective type I interferon production by glial cells in response toFrontiers in immunology · 2025Article
- A positive cytokine/chemokine feedback loop establishes plasmacytoid DC-driven autoimmune pancreatitis in IgG4-related disease.JCI insight · 2024Article
- NOD1: a metabolic modulator.Frontiers in endocrinology · 2024Review
- Reactive Oxygen Species andAntioxidants (Basel, Switzerland) · 2023Review
- Review
- Comprehensive insight into altered host cell-signaling cascades upon Helicobacter pylori and Epstein-Barr virus infections in cancer.Archives of microbiology · 2023Review
82 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular epithelial cell protein known to play a role in host defense at mucosal surfaces. Here we show that a ligand specific for NOD1, a peptide derived from peptidoglycan, initiates an unexpected signaling pathway in human epithelial cell lines that results in the production of type I IFN. Detailed analysis revealed the components of the signaling pathway. NOD1 binding to its ligand triggered activation of the serine-threonine kinase RICK, which was then able to bind TNF receptor-associated factor 3 (TRAF3). This in turn led to activation of TANK-binding kinase 1 (TBK1) and IkappaB kinase epsilon (IKKepsilon) and the subsequent activation of IFN regulatory factor 7 (IRF7). IRF7 induced IFN-beta production, which led to activation of a heterotrimeric transcription factor complex known as IFN-stimulated gene factor 3 (ISGF3) and the subsequent production of CXCL10 and additional type I IFN. In vivo studies showed that mice lacking the receptor for IFN-beta or subjected to gene silencing of the ISGF3 component Stat1 exhibited decreased CXCL10 responses and increased susceptibility to Helicobacter pylori infection, phenotypes observed in NOD1-deficient mice. These studies thus establish that NOD1 can activate the ISGF3 signaling pathway that is usually associated with protection against viral infection to provide mice with robust type I IFN-mediated protection from H. pylori and possibly other mucosal infections.
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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.