ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Nucleotide-binding oligomerization domain 2 signaling promotes hyperresponsive macrophages and colitis in IL-10-deficient mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- LYN and CYBB are pivotal immune and inflammatory genes as diagnostic biomarkers in recurrent spontaneous abortion.Frontiers in immunology · 2025Article
- NOD-like Receptor Signaling Pathway in Gastrointestinal Inflammatory Diseases and Cancers.International journal of molecular sciences · 2023Review
- Blood transcriptome reveals immune and metabolic-related genes involved in growth of pasteurized colostrum-fed calves.Frontiers in genetics · 2023Article
- Loss of NOD2 in macrophages improves colitis and tumorigenesis in a lysozyme-dependent manner.Frontiers in immunology · 2023Article
- NOD-like receptors mediate homeostatic intestinal epithelial barrier function: promising therapeutic targets for inflammatory bowel disease.Therapeutic advances in gastroenterology · 2023Review
- NOD-like receptors in autoimmune diseases.Acta pharmacologica Sinica · 2021Review
- Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections.International journal of molecular sciences · 2021Review
- Intestinal Macrophage Autophagy and its Pharmacological Application in Inflammatory Bowel Disease.Frontiers in pharmacology · 2021Review
- The First Contact of Human Dendritic Cells WithFrontiers in immunology · 2021Article
- The Role of MicroRNAs upon Epithelial-to-Mesenchymal Transition in Inflammatory Bowel Disease.Cells · 2019Review
- B Cell Defects Observed inJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Functional macrophages and gastrointestinal disorders.World journal of gastroenterology · 2018Review
- Genetic deletion of the bacterial sensor NOD2 improves murine Crohn's disease-like ileitis independent of functional dysbiosis.Mucosal immunology · 2017Article
- Microbiota Composition and Immune Responses DuringEuropean journal of microbiology & immunology · 2017Article
- Absence of Nucleotide-Oligomerization-Domain-2 Is Associated with Less Distinct Disease inFrontiers in cellular and infection microbiology · 2017Article
- Immune responses uponGut pathogens · 2017Article
- The role of innate immunity receptors in the pathogenesis of inflammatory bowel disease.Mediators of inflammation · 2015Review
- Nucleotide-binding oligomerization domain-containing protein 2 controls host response to Campylobacter jejuni in Il10-/- mice.The Journal of infectious diseases · 2014Article
- Reactive oxygen species regulate caspase-11 expression and activation of the non-canonical NLRP3 inflammasome during enteric pathogen infection.PLoS pathogens · 2014Article
- NOD2 regulates CXCR3-dependent CD8+ T cell accumulation in intestinal tissues with acute injury.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-10 contributes to the maintenance of intestinal homeostasis via the regulation of inflammatory responses to enteric bacteria. Loss of IL-10 signaling results in spontaneous colitis in mice and early onset enterocolitis in humans. Nucleotide-binding oligomerization domain (NOD) 2 is an intracellular receptor of bacterial peptidoglycan products, and, although NOD2 mutations are associated with Crohn's disease, the precise role of NOD2 in the development of intestinal inflammation remains undefined. To determine the role of NOD2 in the development of colitis on the clinically relevant genetic background of IL-10-deficient signaling, we generated mice lacking IL-10 and NOD2 (IL-10(-/-)NOD2(-/-)). Loss of NOD2 in IL-10(-/-) mice resulted in significant amelioration of chronic colitis, indicating that NOD2 signaling promotes the development of intestinal inflammation in IL-10(-/-) mice. Contrary to previous reports investigating immune function in NOD2(-/-) mice, T cell proliferative capacity and IL-2 production were not impaired, and immune polarization toward type 1 immunity was not affected. However, loss of NOD2 in IL-10-deficient macrophages reduced IL-6, TNF-α, and IL-12p40 production in response to bacterial stimulation. Further analysis of the intrinsic macrophage response before the onset of inflammation revealed that, in the absence of IL-10, synergistic signaling between various TLRs and NOD2 resulted in hyperresponsive, proinflammatory macrophages, thus providing the appropriate immune environment for the development of colitis. Data presented in this study demonstrate that NOD2 signaling contributes to intestinal inflammation that arises through loss of IL-10 and provides mechanistic insight into the development of colitis in inflammatory bowel disease patients with impaired IL-10 signaling.
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