ArticleJournal of leukocyte biology2009
Activation of nucleotide oligomerization domain 2 exacerbates a murine model of proteoglycan-induced arthritis.
Article in Journal of leukocyte biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Uveitis-mediated immune cell invasion through the extracellular matrix of the lens capsule.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Nod2 Deficiency Augments Th17 Responses and Exacerbates Autoimmune Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Simultaneous deletion of NOD1 and NOD2 inhibits in vitro alloresponses but does not prevent allograft rejection.Immunobiology · 2015Article
- Disease severity and mortality can be independently regulated in a mouse model of experimental graft versus host disease.PloS one · 2015Article
- The interrelationship between leukotriene B4 and leukotriene-A4-hydrolase in collagen/adjuvant-induced arthritis in rats.BioMed research international · 2014Article
- Interferon-γ regulates discordant mechanisms of uveitis versus joint and axial disease in a murine model resembling spondylarthritis.Arthritis and rheumatism · 2012Article
- Neutralization of IL-17 ameliorates uveitis but damages photoreceptors in a murine model of spondyloarthritis.Arthritis research & therapy · 2012Article
- 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
- Nucleotide-binding oligomerization domain 2 and Toll-like receptor 2 function independently in a murine model of arthritis triggered by intraarticular peptidoglycan.Arthritis and rheumatism · 2010Article
- Nucleotide oligomerization domain-2 (NOD2)-induced uveitis: dependence on IFN-gamma.Investigative ophthalmology & visual science · 2009Article
- The hidden base of the iceberg: gut peptidoglycome dynamics is foundational to its influence on the host.Gut microbesReview
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
In addition to its role in innate immunity, nucleotide oligomerization domain 2 (NOD2) has been shown to play a suppressive role in models of colitis. Notably, mutations in NOD2 cause the inherited granulomatous disease of the joints called Blau syndrome, thereby linking NOD2 with joint disease as well. However, the role of NOD2 in joint inflammation has not been clarified. We demonstrate here that NOD2 is functional within the mouse joint and promotes inflammation, as locally or systemically administered muramyl dipeptide (MDP; the NOD2 agonist) resulted in significant joint inflammation that was abolished in NOD2-deficient mice. We then sought to investigate the role of NOD2 in a mouse model of inflammatory arthritis dependent on adaptive immunity using TCR-transgenic mice whose T cells recognized the dominant epitope of proteoglycan (PG). Mice immunized with PG in the presence of MDP developed a more severe inflammatory arthritis and histopathology within the joints. Antigen-specific activation of splenocytes was enhanced by MDP with respect to IFN-gamma production, which would be consistent with the Th1-mediated disease in vivo. Intriguingly, NOD2 deficiency did not alter the PG-induced arthritis, indicating that NOD2 does not play an essential role in this model of joint disease when it is not activated by MDP. In conclusion, we demonstrate that in a model of inflammatory arthritis dependent on T and B cell priming, NOD2 activation potentiates disease. However, the absence of NOD2 does not alter the course of inflammatory arthritis, in contrast to models of intestinal inflammation.
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