ArticleNature communications2020
Mucosal-associated invariant T cells promote inflammation and intestinal dysbiosis leading to metabolic dysfunction during obesity.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 154 citations in OpenAlex.
- Review
- Gut archaea drive human MAIT cell responses.bioRxiv : the preprint server for biology · 2026Article
- Article
- MAIT cell plasticity generates CD4Cellular & molecular immunology · 2026Article
- Mucosal-associated invariant T cells and the gut-kidney axis: a review.Clinical kidney journal · 2026Review
- Mucosal-Associated Invariant T (MAIT) Cells in Skin Immunity: Metabolic Regulation, Tissue Adaptation, and Roles in Skin Inflammation and Disease.JID innovations : skin science from molecules to population health · 2026Review
- Unconventional guardians of the brain: MAIT cells as emerging players in glioblastoma immunity.Frontiers in immunology · 2026Review
- Polyphenol-Microbiota Interactions in Atherosclerosis: The Role of Hydroxytyrosol and Tyrosol in Modulating Inflammation and Oxidative Stress.Nutrients · 2025Review
- Intestinal CD4Molecular medicine reports · 2025Article
- Mucosal-Associated Invariant T Cells: Origins, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Microbiome modulation as a therapeutic strategy for alcohol-induced gut dysbiosis and associated disorders.Antonie van Leeuwenhoek · 2025Review
- Metaflammation's Role in Systemic Dysfunction in Obesity: A Comprehensive Review.International journal of molecular sciences · 2025Review
- A prediction nomogram for mild cognitive impairment in type 2 diabetes mellitus based on the Chinese visceral adiposity index.Scientific reports · 2025Article
- Cancer and Cardiovascular Disease: Shared Risk Factors, Mechanisms, and Clinical Implications: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- Development and validation of an inflammatory-based nomogram for predicting arteriovenous fistula maturation failure in end-stage renal disease patients.Langenbeck's archives of surgery · 2025Article
- Insulin resistance as a mediator between obesity and periodontitis risk.BMC oral health · 2025Article
- Mucosal-Associated Invariant T (MAIT) Cell-Mediated Immune Mechanisms of Peritoneal Dialysis-Induced Peritoneal Fibrosis and Therapeutic Targeting.Journal of the American Society of Nephrology : JASN · 2025Article
- Development and validation of Galectin-3 and CVAI-based model for predicting cognitive impairment in type 2 diabetes.Journal of endocrinological investigation · 2025Article
- A charge reversal nano-assembly prevents hepatic steatosis by resolving inflammation and improving lipid metabolism.Bioactive materials · 2025Article
- Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is associated with low-grade chronic inflammation promoting insulin-resistance and diabetes. Gut microbiota dysbiosis is a consequence as well as a driver of obesity and diabetes. Mucosal-associated invariant T cells (MAIT) are innate-like T cells expressing a semi-invariant T cell receptor restricted to the non-classical MHC class I molecule MR1 presenting bacterial ligands. Here we show that during obesity MAIT cells promote inflammation in both adipose tissue and ileum, leading to insulin resistance and impaired glucose and lipid metabolism. MAIT cells act in adipose tissue by inducing M1 macrophage polarization in an MR1-dependent manner and in the gut by inducing microbiota dysbiosis and loss of gut integrity. Both MAIT cell-induced tissue alterations contribute to metabolic dysfunction. Treatment with MAIT cell inhibitory ligand demonstrates its potential as a strategy against inflammation, dysbiosis and metabolic disorders.
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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.