ReviewFrontiers in immunology2022
The Contribution of Neutrophils and NETs to the Development of Type 1 Diabetes.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 41 citations in OpenAlex.
- Negative pressure wound therapy (NPWT) is superior to conventional moist dressings in wound bed preparation for diabetic foot ulcers: A randomized controlled trial.Saudi medical journal · 2023Trial
- Trained immunity: New insights into pathogenesis and therapeutic targets in diabetes and diabetic complications.Genes & diseases · 2026Review
- Neutrophils and neutrophil extracellular traps in diabetes mellitus and its complications: Mechanisms and therapeutic implications.iScience · 2026Review
- Review
- Advances in immune cell-based therapeutic agents for the treatment of inflammation-related diseases.Acta pharmaceutica Sinica. B · 2026Review
- Increased Levels of the Vitamin D Metabolite Ratio Are Protective Against Progression From Islet Autoimmunity to T1D.The Journal of clinical endocrinology and metabolism · 2026Article
- Longitudinal monitoring of type 1 diabetes progression to disease onset.Science advances · 2026Article
- The inflammatory path toward type 1 diabetes begins during pregnancy.Nature communications · 2026Article
- The Gut Microbiota: Emerging Evidence in Autoimmune and Inflammatory Diseases.Research (Washington, D.C.) · 2026Review
- (TCRαβCells · 2025Review
- Neutrophil Extracellular Traps (NETs) in health and disease.Molecular biomedicine · 2025Review
- BAN Score and Distinct Early Cardiometabolic Risk Signatures in a Non-Diabetic Population: A Cross-Sectional Analysis.Healthcare (Basel, Switzerland) · 2025Article
- Multiple low dose streptozotocin-induced diabetes as a model for studying autoimmune diabetes in humans.Animal models and experimental medicine · 2025Review
- The pathophysiology, presentation and classification of Type 1 diabetes.Diabetes, obesity & metabolism · 2025Review
- Antioxidants as Modulators of NETosis: Mechanisms, Evidence, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- NETosis in Autoimmunity: Cell-Mediated vs. Ab-Mediated.Iranian journal of public health · 2025Article
- Neutrophils in Type 1 Diabetes: Untangling the Intricate Web of Pathways and Hypothesis.Biomolecules · 2025Review
- Tissue Resident and Infiltrating Immune Cells: Their Influence on the Demise of Beta Cells in Type 1 Diabetes.Biomolecules · 2025Review
- Review
- The efferocytosis dilemma: how neutrophil extracellular traps and PI3K/Rac1 complicate diabetic wound healing.Cell communication and signaling : CCS · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is an autoimmune disease resulting from the destruction of insulin-producing beta cells in pancreatic islets. T lymphocytes are the claimed pathogenic effectors but abnormalities of other immune cell types, including neutrophils, also characterize T1D development. During human T1D natural history, neutrophils are reduced in the circulation, while accumulate in the pancreas where release of neutrophil extracellular traps (NETs), or NETosis, is manifest. Recent-onset T1D patients also demonstrate activated circulating neutrophils, associated with a unique neutrophil gene signature. Neutrophils can bind to platelets, leading to the formation of platelet-neutrophil aggregates (PNAs). PNAs increase in the circulation during the development of human T1D and provide a mechanism for neutrophil activation and mobilization/recruitment to the pancreas. In non-obese diabetic or NOD mice, T1D autoimmunity is accompanied by dynamic changes in neutrophil numbers, activation state, PNAs and/or NETosis/NET proteins in the circulation, pancreas and/or islets. Such properties differ between stages of T1D disease and underpin potentially indirect and direct impacts of the innate immune system in T1D pathogenesis. Supporting the potential for a pathogenic role in T1D, NETs and extracellular histones can directly damage isolated islets
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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.