ArticleThe Journal of experimental medicine2016
Gut microbiota translocation to the pancreatic lymph nodes triggers NOD2 activation and contributes to T1D onset.
Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.
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Who cites it
112 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.
- Mucosal immune response in biology, disease prevention and treatment.Signal transduction and targeted therapy · 2025Pooled it
- Gut microbiota translocation and dissemination in health: can it be beneficial and purposeful?Gut microbes · 2026Review
- Gut microbiota translocation contributes to early islet apoptosis in streptozotocin-induced diabetes.mSystems · 2026Article
- Article
- Metagenomic Insights into Gut Microbiota Alterations FollowingInternational journal of molecular sciences · 2026Article
- Gut Microbiota and Autoimmune Diseases: The Therapeutic Potential of Probiotics.Current microbiology · 2026Review
- The Gut-Pancreas Axis in Type 1 Diabetes: Emerging Insights into Microbiota and Immune Interactions.International journal of molecular sciences · 2026Review
- Both Gut Microbiota-Dependent and -Independent Constituents of Xinglou Chengqi Decoction Highlight Flavin Adenine Dinucleotide in Treatment of Severe Traumatic Brain Injury.Chinese journal of integrative medicine · 2026Article
- Multiple low dose streptozotocin-induced diabetes as a model for studying autoimmune diabetes in humans.Animal models and experimental medicine · 2025Review
- A plasma metabolomic analysis revealed the metabolic regulatory mechanism of the water extract of Dendrobium huoshanense in improving streptozotocin-induced type 1 diabetes model rats.Journal of natural medicines · 2025Article
- Targeting CD4+ T Cell Glucose Metabolism: A Novel Immunotherapeutic Approach for Type 1 Diabetes.Biomolecules · 2025Review
- Intestinal mucosal immunity and type 1 diabetes: Non-negligible communication between gut and pancreas.Diabetes, obesity & metabolism · 2025Review
- From Microbes to Metabolites: Advances in Gut Microbiome Research in Type 1 Diabetes.Metabolites · 2025Review
- Article
- Microglial Mayhem NLRP3 Inflammasome's Role in Multiple Sclerosis Pathology.CNS neuroscience & therapeutics · 2024Review
- Pathology of Diabetes-Induced Immune Dysfunction.International journal of molecular sciences · 2024Review
- Beneficial In Vitro Effects of Polysaccharide and Non-Polysaccharide Components ofMolecules (Basel, Switzerland) · 2024Article
- Repositioning the Early Pathology of Type 1 Diabetes to the Extraislet Vasculature.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Functional host-specific adaptation of the intestinal microbiome in hominids.Nature communications · 2024Article
- Gut microbiota from B-cell-specific TLR9-deficient NOD mice promote IL-10Frontiers in immunology · 2024Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
Type 1 diabetes (T1D) is an autoimmune disease that is triggered by both genetic and environmental factors, resulting in the destruction of pancreatic β cells. The disruption of the intestinal epithelial barrier and consequent escape of microbial products may be one of these environmental triggers. However, the immune receptors that are activated in this context remain elusive. We show here that during streptozotocin (STZ)-induced T1D, the nucleotide-binding oligomerization domain containing 2 (NOD2), but not NOD1, participates in the pathogenesis of the disease by inducing T helper 1 (Th1) and Th17 cells in the pancreatic LNs (PLNs) and pancreas. Additionally, STZ-injected wild-type (WT) diabetic mice displayed an altered gut microbiota compared with vehicle-injected WT mice, together with the translocation of bacteria to the PLNs. Interestingly, WT mice treated with broad-spectrum antibiotics (Abx) were fully protected from STZ-induced T1D, which correlated with the abrogation of bacterial translocation to the PLNs. Notably, when Abx-treated STZ-injected WT mice received the NOD2 ligand muramyl dipeptide, both hyperglycemia and the proinflammatory immune response were restored. Our results demonstrate that the recognition of bacterial products by NOD2 inside the PLNs contributes to T1D development, establishing a new putative target for intervention during the early stages of the disease.
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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.