ArticleThe Journal of biological chemistry2016
Characterization of Diabetogenic CD8+ T Cells: IMMUNE THERAPY WITH METABOLIC BLOCKADE.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Metabolic Blockade of Glycolysis Diminishes Autoreactive CD4 T-Cell Effector Responses in Type 1 Diabetes.Diabetes · 2026Article
- Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity.Cellular & molecular immunology · 2026Review
- Targeting CD4+ T Cell Glucose Metabolism: A Novel Immunotherapeutic Approach for Type 1 Diabetes.Biomolecules · 2025Review
- Recovery of intracellular glucose uptake in T cells during partial remission of type 1 diabetes.Diabetologia · 2023Article
- T cells in health and disease.Signal transduction and targeted therapy · 2023Review
- Biomarkers of autoimmunity and beta cell metabolism in type 1 diabetes.Frontiers in immunology · 2022Review
- Enhanced T Cell Glucose Uptake Is Associated With Progression of Beta-Cell Function in Type 1 Diabetes.Frontiers in immunology · 2022Article
- New Developments in T Cell Immunometabolism and Therapeutic Implications for Type 1 Diabetes.Frontiers in endocrinology · 2022Review
- The Emerging Role of Immune Cells and Targeted Therapeutic Strategies in Diabetic Wounds Healing.Journal of inflammation research · 2022Review
- Targeting N6-methyladenosine RNA modification combined with immune checkpoint Inhibitors: A new approach for cancer therapy.Computational and structural biotechnology journal · 2022Review
- T-Cell Expression and Release of Kidney Injury Molecule-1 in Response to Glucose Variations Initiates Kidney Injury in Early Diabetes.Diabetes · 2021Article
- Not-so-opposite ends of the spectrum: CD8Nature immunology · 2021Review
- Islet Dysfunction in a Novel Transgenic Model of T Cell Insulitis.Biomolecules · 2021Article
- Targeting Mitochondrial-Derived Reactive Oxygen Species in T Cell-Mediated Autoimmune Diseases.Frontiers in immunology · 2021Review
- Beta cell-specific CD8Nature immunology · 2020Article
- Autoreactive CD8+ T cell exhaustion distinguishes subjects with slow type 1 diabetes progression.The Journal of clinical investigation · 2020Article
- Pharmacological Targeting of GLUT1 to Control Autoreactive T Cell Responses.International journal of molecular sciences · 2019Review
- Targeting Type 1 Diabetes: Selective Approaches for New Therapies.Biochemistry · 2019Review
- Mitochondrial Reactive Oxygen Species and Type 1 Diabetes.Antioxidants & redox signaling · 2018Review
- T-cell Metabolism as a Target to Control Autoreactive T Cells in β-Cell Autoimmunity.Current diabetes reports · 2017Review
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Authors and funding
10 authors at 2 institutions in 1 country.
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Abstract
Type 1 diabetes mellitus is caused by the killing of insulin-producing β cells by CD8+T cells. The disease progression, which is chronic, does not follow a course like responses to conventional antigens such as viruses, but accelerates as glucose tolerance deteriorates. To identify the unique features of the autoimmune effectors that may explain this behavior, we analyzed diabetogenic CD8+ T cells that recognize a peptide from the diabetes antigen IGRP (NRP-V7-reactive) in prediabetic NOD mice and compared them to others that shared their phenotype (CD44(+)CD62L(lo)PD-1(+)CXCR3(+)) but negative for diabetes antigen tetramers and to LCMV (lymphocytic choriomeningitis)-reactive CD8+ T cells. There was an increase in the frequency of the NRP-V7-reactive cells coinciding with the time of glucose intolerance. The T cells persisted in hyperglycemic NOD mice maintained with an insulin pellet despite destruction of β cells. We compared gene expression in the three groups of cells compared with the other two subsets of cells, and the NRP-V7-reactive cells exhibited gene expression of memory precursor effector cells. They had reduced cellular proliferation and were less dependent on oxidative phosphorylation. When prediabetic NOD mice were treated with 2-deoxyglucose to block aerobic glycolysis, there was a reduction in the diabetes antigen versus other cells of similar phenotype and loss of lymphoid cells infiltrating the islets. In addition, treatment of NOD mice with 2-deoxyglucose resulted in improved β cell granularity. These findings identify a link between metabolic disturbances and autoreactive T cells that promotes development of autoimmune diabetes.
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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.