ArticleThe American journal of pathology2011
Autoreactive cytotoxic T lymphocytes acquire higher expression of cytotoxic effector markers in the islets of NOD mice after priming in pancreatic lymph nodes.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Autoreactive T effector memory differentiation mirrors β cell function in type 1 diabetes.The Journal of clinical investigation · 2018Trial
- Flt3L-Derived Antigen-Presenting Cell Transfer in Neonatal NOD Mice Reduces the Incidence of Type 1 Diabetes.Diabetes · 2026Article
- An interleukin-27-centered cytokine circuit regulates macrophage and T cell interactions in autoimmune diabetes.iScience · 2025Article
- JAK inhibitors: a new choice for diabetes mellitus?Diabetology & metabolic syndrome · 2025Review
- An overview of HLA variants in COVID-19 vaccine-induced autoimmunity.International journal of molecular epidemiology and genetics · 2025Review
- Interleukin-27 and Autoimmune Disorders: A Compressive Review of Immunological Functions.Biomolecules · 2024Review
- Analysing the Impact of Resistant Starch Formation in Basmati Rice Products: Exploring Associations with Blood Glucose and Lipid Profiles across Various Cooking and Storage Conditions In Vivo.Foods (Basel, Switzerland) · 2024Article
- Pancreatic draining lymph nodes (PLNs) serve as a pathogenic hub contributing to the development of type 1 diabetes.Cell & bioscience · 2023Review
- Inflammation versus regulation: how interferon-gamma contributes to type 1 diabetes pathogenesis.Frontiers in cell and developmental biology · 2023Review
- Identification of Key Genes and Pathways in Peripheral Blood Mononuclear Cells of Type 1 Diabetes Mellitus by Integrated Bioinformatics Analysis.Diabetes & metabolism journal · 2022Article
- Self-Renewing Islet TCF1Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The healthy exocrine pancreas contains preproinsulin-specific CD8 T cells that attack islets in type 1 diabetes.Science advances · 2020Article
- The JAK1 Selective Inhibitor ABT 317 Blocks Signaling Through Interferon-γ and Common γ Chain Cytokine Receptors to Reverse Autoimmune Diabetes in NOD Mice.Frontiers in immunology · 2020Article
- Interleukin-27 Is Essential for Type 1 Diabetes Development and Sjögren Syndrome-like Inflammation.Cell reports · 2019Article
- IL-21 regulates SOCS1 expression in autoreactive CD8Scientific reports · 2019Article
- Soluble FAS ligand is not required for pancreatic islet inflammation or beta-cell destruction in non-obese diabetic mice.Cell death discovery · 2019Article
- Immune Mechanisms and Pathways Targeted in Type 1 Diabetes.Current diabetes reports · 2018Review
- Type 1 Interferons Potentiate Human CD8Diabetes · 2017Article
- Germinal centre frequency is decreased in pancreatic lymph nodes from individuals with recent-onset type 1 diabetes.Diabetologia · 2017Article
- Neutralization Versus Reinforcement of Proinflammatory Cytokines to Arrest Autoimmunity in Type 1 Diabetes.Clinical reviews in allergy & immunology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Cytotoxic T lymphocytes (CTLs) that cause type 1 diabetes are activated in draining lymph nodes and become concentrated as fully active CTLs in inflamed pancreatic islets. It is unclear whether CTL function is driven by signals received in the lymph node or also in the inflamed tissue. We studied whether the development of cytotoxicity requires further activation in islets. Autoreactive CTLs found in the islets of diabetes-prone NOD mice had acquired much higher expression of the cytotoxic effector markers granzyme B, interferon γ, and CD107a than had those in the pancreatic lymph node (PLN). Increased expression seemed to result from stimulation in the islet itself. T cells held up from migrating from the PLN by administration of the sphingosine-1-phosphate agonist FTY720 did not increase expression of cytotoxic molecules in the PLN. Stimulation did not require antigen presentation or cytokine secretion by the target β cells because it was not affected by the absence of class I major histocompatibility complex expression or by the overexpression of suppressor of cytokine signaling-1. Activation of CD40-expressing cells stimulated increased CTL function and β-cell destruction, suggesting that signals derived from CD40-expressing cells promote the acquisition of cytotoxicity in the islet environment. These data provide in vivo evidence that stimulation of cytotoxic effector molecule expression occurs in inflamed islets and is independent of β cells.
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