ArticlePloS one2013
Nod2 activates NF-kB in CD4+ T cells but its expression is dispensable for T cell-induced colitis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- NOD2 activation reprograms infiltrating inflammatory monocytes in the Zika virus infected CNS to maintain neural correlates of learning and memory.bioRxiv : the preprint server for biology · 2026Article
- Resolving the field: a role for Nod2 in T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- Article
- Lactic Acid Bacteria-Gut-Microbiota-Mediated Intervention towards Inflammatory Bowel Disease.Microorganisms · 2024Review
- NOD2 activation enhances macrophage Fcγ receptor function and may increase the efficacy of antibody therapy.Frontiers in immunology · 2024Article
- Blockade of T cell activation induced by the simultaneous absence of Nod1 and Nod2 is bypassed by TLR2 signals.Transplant immunology · 2021Article
- Article
- Ferroptosis: A Trigger of Proinflammatory State Progression to Immunogenicity in Necroinflammatory Disease.Frontiers in immunology · 2021Review
- T cell-intrinsic role for Nod2 in protection against Th17-mediated uveitis.Nature communications · 2020Article
- NOD2 modulates immune tolerance via the GM-CSF-dependent generation of CD103Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Nutrition, IBD and Gut Microbiota: A Review.Nutrients · 2020Review
- Expression of nucleotide-binding oligomerization domain 1 and 2 in oral lichen planus.Journal of dental sciences · 2020Article
- Beneficial effects of Lactobacillus reuteri 6475 on bone density in male mice is dependent on lymphocytes.Scientific reports · 2019Article
- A Bronze-Tomato Enriched Diet Affects the Intestinal Microbiome under Homeostatic and Inflammatory Conditions.Nutrients · 2018Article
- Nod2 Deficiency Augments Th17 Responses and Exacerbates Autoimmune Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- B Cell Defects Observed inJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- The interplay between microbes and the immune response in inflammatory bowel disease.The Journal of physiology · 2018Review
- Determinants of IBD Heritability: Genes, Bugs, and More.Inflammatory bowel diseases · 2018Review
- Lack of Both Nucleotide-Binding Oligomerization Domain-Containing Proteins 1 and 2 Primes T Cells for Activation-Induced Cell Death.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Methionine restriction on oxidative stress and immune response in dss-induced colitis mice.Oncotarget · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Although the etiology of Crohn's disease (CD) remains elusive this disease is characterized by T cell activation that leads to chronic inflammation and mucosal damage. A potential role for maladaptation between the intestinal microbiota and the mucosal immune response is suggested by the fact that mutations in the pattern recognition receptor Nod2 are associated with higher risks for developing CD. Although Nod2 deletion in CD4(+) T cells has been shown to impair the induction of colitis in the murine T cell transfer model, the analysis of T cell intrinsic Nod2 function in T cell differentiation and T cell-mediated immunity is inconsistent between several studies. In addition, the role of T cell intrinsic Nod2 in regulatory T cell (Treg) development and function during colitis remain to be analyzed. In this study, we show that Nod2 expression is higher in activated/memory CD4(+) T cells and its expression was inducible after T cell receptor (TCR) ligation. Nod2 stimulation with muramyl dipeptide (MDP) led to a nuclear accumulation of c-Rel NF-kB subunit. Although functionally active in CD4(+) T cells, the deletion of Nod2 did not impair the induction and the prevention of colitis in the T cell transfer model. Moreover, Nod2 deletion did not affect the development of Foxp3(+) Treg cells in the spleen of recipient mice and Nod2 deficient CD4 T cells expressing the OVA specific transgenic TCR were able to differentiate in Foxp3(+) Treg cells after OVA feeding. In vitro, CD25(+) Nod2 deficient T cells suppressed T cell proliferation as well as wild type counter parts and T cell stimulation with MDP did not affect the proliferation and the cytokine secretion of T cells. In conclusion, our data indicate that Nod2 is functional in murine CD4(+) T cells but its expression is dispensable for the T cell regulation of colitis.
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