ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Cross-tolerization between Nod1 and Nod2 signaling results in reduced refractoriness to bacterial infection in Nod2-deficient macrophages.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 42 citations in OpenAlex.
- Host response to bacteria induces a shift towards the enteroendocrine cell lineage in the murine enteroid model.PLoS pathogens · 2026Article
- NOD1/NOD2-mediated recognition of non-typeableInnate immunity · 2019Article
- Nucleotide-binding oligomerization domain 1 is dispensable for host immune responses against pulmonary infection ofLaboratory animal research · 2018Article
- E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP.Nature communications · 2017Article
- Nod2: The intestinal gate keeper.PLoS pathogens · 2017Review
- Nucleotide-Binding Oligomerization Domain 2 Contributes to Limiting Growth ofFrontiers in immunology · 2017Article
- Role of nucleotide-binding oligomerization domain 1 (NOD1) and its variants in human cytomegalovirus control in vitro and in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Relevance of the myeloid differentiation factor 88 (MyD88) on RANKL, OPG, and nod expressions induced by TLR and IL-1R signaling in bone marrow stromal cells.Inflammation · 2015Article
- Review
- Emerging significance of NLRs in inflammatory bowel disease.Inflammatory bowel diseases · 2014Review
- Collaborative action of Toll-like and NOD-like receptors as modulators of the inflammatory response to pathogenic bacteria.Mediators of inflammation · 2014Review
- Therapeutic targeting of NOD1 receptors.British journal of pharmacology · 2013Review
- The Interplay between NLRs and Autophagy in Immunity and Inflammation.Frontiers in immunology · 2013Review
- Article
- Roles of NOD1 (NLRC1) and NOD2 (NLRC2) in innate immunity and inflammatory diseases.Bioscience reports · 2012Review
- Farming-associated environmental exposures and effect on atopic diseases.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2012Review
- Nucleotide-binding oligomerization domain 2 (Nod2) is dispensable for the innate immune responses of macrophages against Yersinia enterocolitica.Journal of microbiology (Seoul, Korea) · 2012Article
- Immunological and inflammatory responses to organic dust in agriculture.Current opinion in allergy and clinical immunology · 2012Review
- Pathogen-mediated proteolysis of the cell death regulator RIPK1 and the host defense modulator RIPK2 in human aortic endothelial cells.PLoS pathogens · 2012Article
- Organic dust augments nucleotide-binding oligomerization domain expression via an NF-{kappa}B pathway to negatively regulate inflammatory responses.American journal of physiology. Lung cellular and molecular physiology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Nod2 is an intracellular innate immune receptor that plays a role in host defense and susceptibility to inflammatory disease. We show in this study that macrophages rendered refractory to TLR4 and Nod2 signaling by exposure to LPS and muramyl dipeptide (MDP) exhibit impaired TNF-alpha and IL-6 production in response to pathogenic Listeria monocytogenes and Yersinia pseudotuberculosis as well as commensal bacteria including Escherichia coli and Bacteroides fragilis. Surprisingly, Nod2 deficiency was associated with impaired tolerization in response to pathogenic and commensal bacteria. Mechanistically, reduced tolerization of Nod2-null macrophages was mediated by recognition of bacteria through Nod1 because it was abolished in macrophages deficient in Nod1 and Nod2. Consistently, Nod2-null macrophages tolerant to LPS and MDP showed enhanced production of TNF-alpha and IL-6 as well as increased NF-kappaB and MAPK activation in response to the dipeptide KF1B, the Nod1 agonist. Furthermore, reduced tolerization of Nod2-deficient macrophages in response to bacteria was abolished when mutant macrophages were also rendered tolerant to the Nod1 ligand. Finally, MDP stimulation induced refractoriness not only to MDP, but also to iE-DAP stimulation, providing a mechanism to explain the reduced tolerization of Nod2-deficient macrophages infected with bacteria. These results demonstrate that cross-tolerization between Nod1 and Nod2 leads to increase recognition of both pathogenic and commensal bacteria in Nod2-deficient macrophages pre-exposed to microbial ligands.
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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.