ArticleProceedings of the National Academy of Sciences of the United States of America2008
Differential function of the NACHT-LRR (NLR) members Nod1 and Nod2 in arthritis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 63 citations in OpenAlex.
- Review
- Review
- NOD1 deficiency promotes inflammation via autophagic degradation of ASK1.Communications biology · 2025Article
- FOCUS on NOD2: Advancing IBD Drug Discovery with a User-Informed Machine Learning Framework.ACS medicinal chemistry letters · 2024Article
- Strong association of common variants in the miRNA-binding site of NOD2 gene with clinicopathological characteristics and disease activity of systemic lupus erythematosus.Clinical rheumatology · 2021Article
- Review
- Synergistic Activation of Toll-Like and NOD Receptors by Complementary Antigens as Facilitators of Autoimmune Disease: Review, Model and Novel Predictions.International journal of molecular sciences · 2020Review
- NOD2 signaling pathway is involved in fibronectin fragment-induced pro-catabolic factor expressions in human articular chondrocytes.BMB reports · 2019Article
- Article
- Nod2 Deficiency Augments Th17 Responses and Exacerbates Autoimmune Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Genetic deficiency of NOD2 confers resistance to invasive aspergillosis.Nature communications · 2018Article
- The Absence of NOD1 Enhances Killing ofFrontiers in immunology · 2017Article
- The Role of the Transcriptional Regulation of Stromal Cells in Chronic Inflammation.Biomolecules · 2015Review
- NOD proteins: regulators of inflammation in health and disease.Nature reviews. Immunology · 2014Review
- RIP2 activity in inflammatory disease and implications for novel therapeutics.Journal of leukocyte biology · 2013Review
- Immune modulation by different types of β2→1-fructans is toll-like receptor dependent.PloS one · 2013Article
- NOD2 is highly expressed in Behçet disease with pulmonary manifestations.Journal of inflammation (London, England) · 2012Article
- Immunopathological roles of cytokines, chemokines, signaling molecules, and pattern-recognition receptors in systemic lupus erythematosus.Clinical & developmental immunology · 2012Review
- NOD1 and NOD2 Signaling in Infection and Inflammation.Frontiers in immunology · 2012Article
- Temporal dynamics of host molecular responses differentiate symptomatic and asymptomatic influenza a infection.PLoS genetics · 2011Article
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of chronic joint inflammation remains unclear, although the involvement of pathogen recognition receptors has been suggested recently. In the present article, we describe the role of two members of the NACHT-LRR (NLR) family, Nod1 (nucleotide-binding oligomerization domain) and Nod2 in a model of acute joint inflammation induced by intraarticular injection of Streptococcus pyogenes cell wall fragments. Here, we show that Nod2 deficiency resulted in reduced joint inflammation and protection against early cartilage damage. In contrast, Nod1 gene-deficient mice developed enhanced joint inflammation with concomitant elevated levels of proinflammatory cytokines and cartilage damage, consistent with a model in which Nod1 controls the inflammatory reaction. To explore whether the different function of Nod1 and Nod2 occurs also in humans, we exposed peripheral blood mononuclear cells (PBMCs) carrying either Nod1ins/del or Nod2fs mutation with SCW fragments in vitro. Production of both TNFalpha and IL-1beta was clearly impaired in PBMCs carrying the Nod2fs compared with PBMCs isolated from healthy controls. In line with results in Nod1 gene-deficient mice, PBMCs from individuals bearing a newly described Nod1 mutation produced enhanced levels of proinflammatory cytokines after 24-h stimulation with SCW fragments. These data indicate that the NLR family members Nod1 and Nod2 have different functions in controlling inflammation, and that intracellular Nod1-Nod2 interactions may determine the severity of arthritis in this experimental model. Whether a distorted balance between the function of Nod1 and/or Nod2 is involved in the pathogenesis of human autoinflammatory or autoimmune disease, such as rheumatoid arthritis, remains to be elucidated.
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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 OpenQuestion graph.