ArticleFrontiers in immunology2023
Loss of NOD2 in macrophages improves colitis and tumorigenesis in a lysozyme-dependent manner.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Inflammatory bowel disease treatment: Mechanisms to clinical translation (Review).International journal of molecular medicine · 2026Review
- Shikonin Modulates the NOD2/CARD9 Pathway to Ameliorate Ulcerative Colitis Through Inhibiting M1 Macrophage Polarization.Applied biochemistry and biotechnology · 2025Article
- Innate immunity in tumors: roles and therapeutic targets.Frontiers in immunology · 2025Review
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Crohn's disease (CD) is a complex and poorly understood myeloid-mediated disorder. Genetic variants with loss of function in the Methods: To ablate Nod2 specifically within the myeloid compartment, we generated Results: Upon DSS colitis model, Conclusion: Our results indicate that loss of Nod2 signaling in myeloid cells aids in the tissue repair of the inflamed large intestine through lysozyme secretion by myeloid cells. These results may pave the way to design new therapeutics to limit the inflammatory and tumorigenic functions of NOD2.
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Registered trials
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