ArticleJournal of immunology (Baltimore, Md. : 1950)2014
NOD2 regulates CXCR3-dependent CD8+ T cell accumulation in intestinal tissues with acute injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02721719 (The Role of CD4+ T Cell Subsets in the Mechanism of Action of Vedolizumab in Ulcerative Colitis), which is not on this map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
The Role of CD4+ T Cell Subsets in the Mechanism of Action of Vedolizumab in Ulcerative Colitis
Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
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- T cell-intrinsic role for Nod2 in protection against Th17-mediated uveitis.Nature communications · 2020Article
- Myeloid Cell Expression of LACC1 Is Required for Bacterial Clearance and Control of Intestinal Inflammation.Gastroenterology · 2020Article
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- Role of CXCR3 signaling in response to anti-PD-1 therapy.EBioMedicine · 2019Article
- CNS lymphatic drainage and neuroinflammation are regulated by meningeal lymphatic vasculature.Nature neuroscience · 2018Article
- Nod2 Deficiency Augments Th17 Responses and Exacerbates Autoimmune Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Trigger-happy resident memory CD4Mucosal immunology · 2018Article
- Human stem cells home to and repair laser-damaged trabecular meshwork in a mouse model.Communications biology · 2018Article
- JAK2 Disease-Risk Variants Are Gain of Function and JAK Signaling Threshold Determines Innate Receptor-Induced Proinflammatory Cytokine Secretion in Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- STAT3 in CD8+ T Cells Inhibits Their Tumor Accumulation by Downregulating CXCR3/CXCL10 Axis.Cancer immunology research · 2015Article
- Twist1 and Twist2 Contribute to Cytokine Downregulation following Chronic NOD2 Stimulation of Human Macrophages through the Coordinated Regulation of Transcriptional Repressors and Activators.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Intestinal barrier loss as a critical pathogenic link between inflammatory bowel disease and graft-versus-host disease.Mucosal immunology · 2015Review
- Activation of pattern recognition receptors up-regulates metallothioneins, thereby increasing intracellular accumulation of zinc, autophagy, and bacterial clearance by macrophages.Gastroenterology · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Polymorphisms in NOD2 confer risk for Crohn's disease, characterized by intestinal inflammation. How NOD2 regulates both inflammatory and regulatory intestinal T cells, which are critical to intestinal immune homeostasis, is not well understood. Anti-CD3 mAb administration is used as therapy in human autoimmune diseases, as well as a model of transient intestinal injury. The stages of T cell activation, intestinal injury, and subsequent T tolerance are dependent on migration of T cells into the small intestinal (SI) lamina propria. Upon anti-CD3 mAb treatment of mice, we found that NOD2 was required for optimal small intestinal IL-10 production, in particular from CD8(+) T cells. This requirement was associated with a critical role for NOD2 in SI CD8(+) T cell accumulation and induction of the CXCR3 ligands CXCL9 and CXCL10, which regulate T cell migration. NOD2 was required in both the hematopoietic and nonhematopoietic compartments for optimal expression of CXCR3 ligands in intestinal tissues. NOD2 synergized with IFN-γ to induce CXCL9 and CXCL10 secretion in dendritic cells, macrophages, and intestinal stromal cells in vitro. Consistent with the in vitro studies, during anti-CD3 mAb treatment in vivo, CXCR3 blockade, CD8(+) T cell depletion, or IFN-γ neutralization each inhibited SI CD8(+) T cell recruitment, and reduced chemokine expression and IL-10 expression. Thus, NOD2 synergizes with IFN-γ to promote CXCL9 and CXCL10 expression, thereby amplifying CXCR3-dependent SI CD8(+) T cell migration during T cell activation, which, in turn, contributes to induction of both inflammatory and regulatory T cell outcomes in the intestinal environment.
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Registered trials
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.