ArticleArthritis and rheumatism2010
Nucleotide-binding oligomerization domain 2 and Toll-like receptor 2 function independently in a murine model of arthritis triggered by intraarticular peptidoglycan.
Article in Arthritis and rheumatism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Macroglobulinemia and Autoinflammatory Disease.Rheumatology and immunology research · 2021Review
- Interplay between Peptidoglycan Biology and Virulence in Gram-Negative Pathogens.Microbiology and molecular biology reviews : MMBR · 2018Review
- Nod2 Deficiency Augments Th17 Responses and Exacerbates Autoimmune Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Identification of Potent and Selective RIPK2 Inhibitors for the Treatment of Inflammatory Diseases.ACS medicinal chemistry letters · 2017Article
- Mycobacterium tuberculosis promotes arthritis development through Toll-like receptor 2.Journal of bone and mineral metabolism · 2015Article
- Blau syndrome-associated Nod2 mutation alters expression of full-length NOD2 and limits responses to muramyl dipeptide in knock-in mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Article
- In vivo inhibition of RIPK2 kinase alleviates inflammatory disease.The Journal of biological chemistry · 2014Article
- NOD proteins: regulators of inflammation in health and disease.Nature reviews. Immunology · 2014Review
- Emerging role of endosomal toll-like receptors in rheumatoid arthritis.Frontiers in immunology · 2014Review
- TLR2 elicits IL-17-mediated RANKL expression, IL-17, and OPG production in neutrophils from arthritic mice.Mediators of inflammation · 2014Article
- TLR2 deletion promotes arthritis through reduction of IL-10.Journal of leukocyte biology · 2013Article
- Investigation of the peptidoglycan sensing molecule, PGLYRP-2, in murine inflammatory uveitis.The British journal of ophthalmology · 2013Article
- Impact of IL-1 signalling on experimental uveitis and arthritis.Annals of the rheumatic diseases · 2012Article
- Neutralization of IL-17 ameliorates uveitis but damages photoreceptors in a murine model of spondyloarthritis.Arthritis research & therapy · 2012Article
- Nod2: a key regulator linking microbiota to intestinal mucosal immunity.Journal of molecular medicine (Berlin, Germany) · 2012Review
- NLRs in immune privileged sites.Current opinion in pharmacology · 2011Review
- Dectin-1 and NOD2 mediate cathepsin activation in zymosan-induced arthritis in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- NOD2 deficiency results in increased susceptibility to peptidoglycan-induced uveitis in mice.Investigative ophthalmology & visual science · 2011Article
- Aberrant interleukin-1 signalling does not increase susceptibility of mice to NOD2-dependent uveitis.Clinical & experimental ophthalmologyArticle
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6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveBlau syndrome is an autoinflammatory disease resulting from mutations in the NOD2 gene, wherein granulomatous arthritis, uveitis, and dermatitis develop. The mechanisms by which aberrant NOD2 causes joint inflammation are poorly understood. Indeed, very few studies have addressed the function of nucleotide-binding oligomerization domain 2 (NOD-2) in the joint. This study was undertaken to investigate NOD-2 function in an experimental model of arthritis and to explore the potential interplay between Toll-like receptor 2 (TLR-2) and NOD-2 in joint inflammation.
methodsMice deficient in TLR-2, myeloid differentiation factor 88 (MyD88), or NOD-2 and their wild-type controls were given an intraarticular injection of muramyl dipeptide (MDP), peptidoglycan (PG; a metabolite of which is MDP), or palmitoyl-3-cysteine-serine-lysine-4 (Pam(3)CSK(4)), a synthetic TLR-2 agonist. Joint inflammation was assessed by near-infrared fluorescence imaging and histologic analysis.
resultsLocally administered PG resulted in joint inflammation, which was markedly reduced in mice deficient in either TLR-2 or the TLR signaling mediator MyD88. In addition to TLR-2 signaling events, NOD-2 mediated joint inflammation, as evidenced by the fact that mice deficient in NOD-2 showed significantly reduced PG-induced arthritis. TLR-2 or MyD88 deficiency did not influence arthritis induced by the specific NOD-2 agonist MDP. In addition, NOD-2 deficiency did not alter the TLR-2-dependent joint inflammation elicited by the synthetic TLR-2 agonist Pam(3)CSK(4).
conclusionWhereas NOD-2 and TLR-2 are both critical for the development of PG-induced arthritis, they appear to elicit inflammation independently of each other. Our findings indicate that NOD-2 plays an inflammatory role in arthritis.
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