ArticlePloS one2017
Programmed cell death-1, PD-1, is dysregulated in T cells from children with new onset type 1 diabetes.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Immune checkpoint inhibitors and type 1 diabetes mellitus: a case report and systematic review.European journal of endocrinology · 2019Pooled it
- Autoantibody-positive healthy individuals with lower lupus risk display a unique immune endotype.The Journal of allergy and clinical immunology · 2020Trial
- CAR T cell therapy in type 1 diabetes: what we know and what remains to be explored.Biological procedures online · 2025Review
- Beta cell extracellular vesicle PD-L1 as a novel regulator of CD8Diabetologia · 2025Article
- Inflammasome activation and accelerated immune aging in autoimmune disorders.Frontiers in aging · 2025Article
- Beta cell extracellular vesicle PD-L1 as a novel regulator of CD8+ T cell activity and biomarker during the evolution of Type 1 Diabetes.bioRxiv : the preprint server for biology · 2024Article
- Recovery of intracellular glucose uptake in T cells during partial remission of type 1 diabetes.Diabetologia · 2023Article
- Altered Fatty Acid Oxidation in Lymphocyte Populations of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2023Article
- New-onset type 1 diabetes mellitus as a delayed immune-related event after discontinuation of nivolumab: A case report.Medicine · 2022Article
- Immune checkpoint inhibitor-induced diabetes mellitus with pembrolizumab.BMJ case reports · 2022Article
- Human CD4Frontiers in immunology · 2022Article
- Physical activity and exercise as an essential medical strategy for the COVID-19 pandemic and beyond.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Immune Checkpoint Inhibitor-Induced Diabetes Mellitus: Potential Role of T Cells in the Underlying Mechanism.International journal of molecular sciences · 2021Review
- Integrative computational approach identifies drug targets in CD4NPJ systems biology and applications · 2021Article
- Unravelling Checkpoint Inhibitor Associated Autoimmune Diabetes: From Bench to Bedside.Frontiers in endocrinology · 2021Review
- Glycolysis Inhibition Induces Functional and Metabolic Exhaustion of CD4Frontiers in immunology · 2021Article
- Cases from the Immune-Related Adverse Event Tumor Board: Diagnosis and Management of Immune Checkpoint Blockade-Induced Diabetes.The oncologist · 2020Article
- Management of endocrine immune-related adverse events of immune checkpoint inhibitors: an updated review.Endocrine connections · 2020Review
- High intensity interval exercise increases the frequency of peripheral PD-1+ CD8Brain, behavior, & immunity - health · 2020Article
- Role of the PD-1/PD-L1 Dyad in the Maintenance of Pancreatic Immune Tolerance for Prevention of Type 1 Diabetes.Frontiers in endocrinology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProgrammed death cell 1 (PD-1) is an inhibitor of T cell activation and is also functionally linked to glycolysis. We hypothesized that PD-1 expression is defective in activated T cells from children with type 1 diabetes (T1D), resulting in abnormal T cell glucose metabolism.
methodsIn this pilot study, we enrolled children with new onset T1D within 2 weeks of diagnosis (T1D), unaffected siblings of T1D (SIBS), unaffected, unrelated children (CTRL), children with new onset, and untreated Crohn disease (CD). We repeated the assays 4-6 months post-diagnosis in T1D (T1D follow up). We analyzed anti-CD3/-CD28-stimulated peripheral blood mononuclear cells (PBMC) subsets for PD-1 expression by flow cytometry at baseline and after 24 h in culture. We measured cytokines in the culture medium by multiplex ELISA and glycolytic capacity with a flux analyzer.
resultsWe enrolled 37 children. T cells derived from subjects with T1D had decreased PD-1 expression compared to the other study groups. However, in T1D follow-up T cells expressed PD-1 similarly to controls, but had no differences in PBMC cytokine production. Nonetheless, T1D follow up PBMCs had enhanced glycolytic capacity compared to T1D.
conclusionsActivated T cells from T1D fail to upregulate PD-1 upon T-cell receptor stimulation, which may contribute to the pathogenesis of T1D. T1D follow up PBMC expression of PD-1 normalizes, together with a significant increase in glycolysis compared to T1D. Thus, insulin therapy in T1D children is associated with normal PD1 expression and heightened glycolytic capacity in PBMC.
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