ArticleDiabetes2023
Inflammatory Cell Infiltration Into Islets Without PD-L1 Expression Is Associated With the Development of Immune Checkpoint Inhibitor-Related Type 1 Diabetes in Genetically Susceptible Patients.
Article in Diabetes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- Type 3 Autoimmune Pancreatitis: What Do We Know So Far?Digestive diseases and sciences · 2026Review
- Article
- Immune checkpoints and immunoregulation in metabolic diseases and cancers: pathological mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2026Review
- Immune checkpoint inhibitor-related endocrinopathies: from immune crosstalk to predictive biomarkers and precision management.Frontiers in endocrinology · 2026Review
- Association between HLA-DRB1*04:05 and the efficacy of immune checkpoint inhibitors for patients with advanced cancer.Frontiers in endocrinology · 2026Article
- Macrophage-mediated metabolic dysregulation in the pancreas: Insights from obesity.World journal of biological chemistry · 2025Review
- Autoimmune origin for immune checkpoint inhibitor-diabetes revealed by deep immune phenotyping of the pancreas.Journal for immunotherapy of cancer · 2025Article
- Risk Factors Associated with the Development of Immune-Checkpoint Inhibitor Diabetes Mellitus: An Integrative Review.Life (Basel, Switzerland) · 2025Review
- Immune checkpoint inhibitor-related diabetes mellitus associated with high signal intensity in diffusion-weighted magnetic resonance imaging of the pancreas at an early clinical stage.Hormones (Athens, Greece) · 2025Article
- Management, biomarkers and prognosis in people developing endocrinopathies associated with immune checkpoint inhibitors.Nature reviews. Endocrinology · 2025Review
- Immune checkpoint inhibitor-related type 1 diabetes mellitus with closely monitored dynamics of glutamic acid decarboxylase antibody levels before and after disease onset.Diabetology international · 2025Article
- Beta cell extracellular vesicle PD-L1 as a novel regulator of CD8Diabetologia · 2025Article
- Cemiplimab and diabetic ketoacidosis: a case report of a rare endocrinopathy associated with immune checkpoint inhibitors.Frontiers in endocrinology · 2025Article
- Endoscopic Ultrasound With Fine Needle Biopsy Confirming a Diagnosis of Immune Checkpoint Inhibitor-Related Type 3 Autoimmune Pancreatitis.Case reports in gastrointestinal medicine · 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
- Immune checkpoint inhibitor-related type 1 diabetes mellitus which develops long after treatment discontinuation: a case report and review of literature.Diabetology international · 2024Article
- Inhibition of the eukaryotic initiation factor-2α kinase PERK decreases risk of autoimmune diabetes in mice.The Journal of clinical investigation · 2024Article
- Inhibition of the Eukaryotic Initiation Factor-2-α Kinase PERK Decreases Risk of Autoimmune Diabetes in Mice.bioRxiv : the preprint server for biology · 2024Article
- Reaching the Diagnosis of Checkpoint Inhibitor-Induced Diabetes Mellitus in Different Clinical Scenarios: A Real-World Application of Updated Diagnostic Criteria.Diseases (Basel, Switzerland) · 2024Article
- Case report: Strong GAD antibody positivity and type 1 diabetes-HLA-susceptible haplotype-DRB1*04:05-DQB1*04:01 in a Japanese patient with immune checkpoint inhibitor-induced type 1 diabetes.Frontiers in endocrinology · 2024Article
Corrections and comments
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Authors and funding
20 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune checkpoint inhibitors (ICIs) could cause type 1 diabetes (T1D). However, the underlying mechanism remains unclear. We immunohistochemically analyzed pancreatic specimens from three individuals with ICI-related T1D, and their histopathological data were compared those from three patients who had received ICI therapy but did not develop T1D (non-T1D) and seven normal glucose-tolerant subjects as control subjects. All ICI-related T1D patients had susceptible HLA haplotypes. In ICI-related T1D, the β-cell area decreased and the α-cell area increased compared with non-T1D and control subjects. The number of CD3-positive cells around islets increased in ICI-related T1D and non-T1D compared with control subjects, while the number of CD68-positive cells around islets increased in ICI-related T1D compared with non-T1D and control subjects. The expression ratios of programmed death-ligand 1 (PD-L1) on islets decreased in non-T1D and almost completely disappeared in ICI-related T1D, while PD-L1 expression was observed in most cells of pancreatic islets in control subjects. This study, therefore, indicates that ICI therapy itself could reduce PD-L1 expression on islets in all subjects, which may be related to β-cell vulnerability. In addition, we showed that absence of PD-L1 expression on β-cells, genetic susceptibility, and infiltration of macrophages as well as T lymphocytes around islets might be responsible for T1D onset. ARTICLE HIGHLIGHTS:
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