ArticleFrontiers in immunology2020
NOD2 Deficiency Promotes Intestinal CD4+ T Lymphocyte Imbalance, Metainflammation, and Aggravates Type 2 Diabetes in Murine Model.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Association of gastrointestinal microbiome and obesity with gestational diabetes mellitus-an updated globally based review of the high-quality literatures.Nutrition & diabetes · 2024Pooled it
- Graph in Graph (GiG): A novel graph AI framework for integrating and interpreting medical and omics data.bioRxiv : the preprint server for biology · 2026Article
- Intestinal-related substances in obesity regulation: A comprehensive review.World journal of gastrointestinal pharmacology and therapeutics · 2025Review
- Resolving the field: a role for Nod2 in T cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Review
- Common inherited loss-of-function mutations in the innate sensor NOD2 contribute to exceptional immune response to cancer immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Changes of intestinal microbiome and its relationship with painful diabetic neuropathy in rats.BMC microbiology · 2025Article
- Autophagy in inflammatory bowel disease: immunization, etiology, and therapeutic potential.Frontiers in immunology · 2025Review
- NOD1 and NOD2: Essential Monitoring Partners in the Innate Immune System.Current issues in molecular biology · 2024Review
- Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Role of pattern recognition receptors and microbiota-derived ligands in obesity.Frontiers in microbiomes · 2024Review
- Electroacupuncture Reduces Inflammatory Bowel Disease in Obese Mice by Activating the Nrf2/HO-1 Signaling Pathways and Repairing the Intestinal Barrier.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- The characteristics of intestinal microbiota in patients with type 2 diabetes and the correlation with the percentage of T-helper cells.Frontiers in microbiology · 2024Article
- The visceral adipose tissue bacterial microbiota provides a signature of obesity based on inferred metagenomic functions.International journal of obesity (2005) · 2023Article
- NOD-like Receptors-Emerging Links to Obesity and Associated Morbidities.International journal of molecular sciences · 2023Review
- Role ofNutrients · 2023Review
- Population-enriched innate immune variants may identify candidate gene targets at the intersection of cancer and cardio-metabolic disease.Frontiers in endocrinology · 2023Review
- Mechanisms of gut microbiota-immune-host interaction on glucose regulation in type 2 diabetes.Frontiers in microbiology · 2023Review
- Article
- Network Pharmacology and Transcriptomics Reveal the Mechanism of GuaLouQuMaiWan in Treatment of Type 2 Diabetes and Its Active Small Molecular Compound.Journal of diabetes research · 2022Article
- The role of Th17 cells in endocrine organs: Involvement of the gut, adipose tissue, liver and bone.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes (T2D) is a metabolic disease characterized by increased inflammation, NOD-like receptors (NLRs) activation and gut dysbiosis. Our research group has recently reported that intestinal Th17 response limits gut dysbiosis and LPS translocation to visceral adipose tissue (VAT), protecting against metabolic syndrome. However, whether NOD2 receptor contributes intestinal Th17 immunity, modulates dysbiosis-driven metabolic tissue inflammation, and obesity-induced T2D remain poorly understood. In this context, we observed that mice lacking NOD2 fed a high-fat diet (HFD) display severe obesity, exhibit greater adiposity, and more hepatic steatosis compared to HFD-fed wild-type (WT) mice. In addition, they develop increased hyperglycemia, worsening of glucose intolerance, and insulin resistance. Notably, the deficiency of NOD2 causes a deviation from M2 macrophage and regulatory T cells (Treg) to M1 macrophage and mast cells into VAT compared to WT mice fed HFD. An imbalance was also observed in Th17/Th1 cell populations, with reduced IL-17 and IL-22 gene expression in the mesenteric lymph nodes (MLNs) and ileum, respectively, of NOD2-deficient mice fed HFD. 16S rRNA sequencing indicates lower richness, alpha diversity, and a depletion of
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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.