ArticleInvestigative ophthalmology & visual science2011
NOD2 deficiency results in increased susceptibility to peptidoglycan-induced uveitis in mice.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Immunological analysis of Blau syndrome, a unique autoinflammatory state.Frontiers in immunology · 2026Review
- Crosstalk between NOD2 and TLR2 suppresses the development of TLR2-mediated experimental colitis.Journal of clinical biochemistry and nutrition · 2024Article
- Blau syndrome NOD2 mutations result in loss of NOD2 cross-regulatory function.Frontiers in immunology · 2022Article
- Macroglobulinemia and Autoinflammatory Disease.Rheumatology and immunology research · 2021Review
- Real-Time Imaging of Immune Modulation by Cannabinoids Using Intravital Fluorescence Microscopy.Cannabis and cannabinoid research · 2021Review
- Dysbiosis From a Microbial and Host Perspective Relative to Oral Health and Disease.Frontiers in microbiology · 2021Review
- Whole-Exome Sequencing of Patients With Posterior Segment Uveitis.American journal of ophthalmology · 2021Article
- Phenotypic Differences in Primary Murine Microglia Treated with NOD1, NOD2, and NOD1/2 Agonists.Journal of molecular neuroscience : MN · 2020Article
- The common NOD2/CARD15 variant P268S in patients with non-infectious uveitis: a cohort study.Pediatric rheumatology online journal · 2015Article
- Acute Anterior Uveitis and Spondyloarthritis: More Than Meets the Eye.Current rheumatology reports · 2015Review
- Holding the inflammatory system in check: NLRs keep it cool.F1000prime reports · 2015Review
- Investigation of the peptidoglycan sensing molecule, PGLYRP-2, in murine inflammatory uveitis.The British journal of ophthalmology · 2013Article
- Uveitis in seronegative arthritis.Current rheumatology reports · 2012Review
- Investigation of the differential potentials of TLR agonists to elicit uveitis in mice.Journal of leukocyte biology · 2011Article
- NLRs in immune privileged sites.Current opinion in pharmacology · 2011Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
purposeThe innate immune receptor NOD2 is a genetic cause of uveitis (Blau syndrome). Intriguingly, in the intestine where polymorphisms of NOD2 predispose to Crohn's disease, NOD2 reportedly suppresses inflammation triggered by the bacterial cell wall component, peptidoglycan (PGN). Whether NOD2 exerts a similar capacity in the regulation of ocular inflammation to PGN has not been explored.
methodsNOD2, NOD1, or MyD88 knockout (KO) mice and their wild-type (WT) controls were administered an intravitreal injection of PGN (a metabolite of which is the NOD2 agonist, muramyl dipeptide), or synthetic TLR2/1 and TLR2/6 agonists, Pam₃CSK4 and FSL-1. Ocular inflammation was assessed by intravital microscopy and histopathology. Cytokine production in eye tissue homogenates was measured by ELISA.
resultsPGN triggered uveitis in mice. This inflammation was abolished in the absence of the TLR signaling mediator MyD88. NOD2 exerted a negative regulatory role because PGN-triggered eye inflammation was exacerbated in NOD2 KO mice. Increased intravascular response coincided with enhanced leukocytes within the aqueous and vitreous humors. The enhanced susceptibility of NOD2 KO mice to PGN uveitis coincided with increased cytokine production of IL-12p40, IL-17, and IL-23 but not IL-12p70, TNFα, or IFNγ. NOD1 deficiency did not result in the same sensitivity to PGN. Ocular inflammation induced by synthetic TLR2 agonists required MyD88 but not NOD2 or NOD1.
conclusionsNOD2 may serve differential roles in the eye to promote inflammation while also tempering cell responses to PGN akin to what has been reported in colitis.
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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 Socratic graph.