ArticleEMBO molecular medicine2012
A guanidine-rich regulatory oligodeoxynucleotide improves type-2 diabetes in obese mice by blocking T-cell differentiation.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Case report: A diabetic patient with cryptococcal meningoencephalitis complicated by post-infectious inflammatory response syndrome.Frontiers in immunology · 2024Article
- The Alterations in and the Role of the Th17/Treg Balance in Metabolic Diseases.Frontiers in immunology · 2021Review
- Multiple genetic variants associated with posttransplantation diabetes mellitus in Chinese Han populations.Journal of clinical laboratory analysis · 2018Article
- Integrated genomic and prospective clinical studies show the importance of modular pleiotropy for disease susceptibility, diagnosis and treatment.Genome medicine · 2014Article
- The interplay between regulatory T cells and metabolism in immune regulation.Oncoimmunology · 2013Review
- Immunological goings-on in visceral adipose tissue.Cell metabolism · 2013Review
- Participation of leptin in the determination of the macrophage phenotype: an additional role in adipocyte and macrophage crosstalk.In vitro cellular & developmental biology. Animal · 2013Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
T lymphocytes exhibit pro-inflammatory or anti-inflammatory activities in obesity and diabetes, depending on their subtypes. Guanidine-rich immunosuppressive oligodeoxynucleotides (ODNs) effectively control Th1/Th2-cell counterbalance. This study reveals a non-toxic regulatory ODN (ODNR01) that inhibits Th1- and Th17-cell polarization by binding to STAT1/3/4 and blocking their phosphorylation without affecting Th2 and regulatory T cells. ODNR01 improves glucose tolerance and insulin sensitivity in both diet-induced obese (DIO) and genetically generated obese (ob/ob) mice. Mechanistic studies show that ODNR01 suppresses Th1- and Th17-cell differentiation in white adipose tissue, thereby reducing macrophage accumulation and M1 macrophage inflammatory molecule expression without affecting M2 macrophages. While ODNR01 shows no effect on diabetes in lymphocyte-free Rag1-deficient DIO mice, it enhances glucose tolerance and insulin sensitivity in CD4(+) T-cell-reconstituted Rag1-deficient DIO mice, suggesting its beneficial effect on insulin resistance is T-cell-dependent. Therefore, regulatory ODNR01 reduces obesity-associated insulin resistance through modulation of T-cell differentiation.
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Registered trials
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