ArticleJournal of autoimmunity2011
IL-18 is required for self-reactive T cell expansion in NOD mice.
Article in Journal of autoimmunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Review
- Exploring Computational Data Amplification and Imputation for the Discovery of Type 1 Diabetes (T1D) Biomarkers from Limited Human Datasets.Biomolecules · 2022Article
- Interleukin-18 cytokine in immunity, inflammation, and autoimmunity: Biological role in induction, regulation, and treatment.Frontiers in immunology · 2022Review
- Interleukin-18 in metabolism: From mice physiology to human diseases.Frontiers in endocrinology · 2022Review
- Inflammasomes and Type 1 Diabetes.Frontiers in immunology · 2021Review
- Epigenetic modulation of selected immune response genes and altered functions of T lymphocytes and macrophages collectively contribute to autoimmune diabetes protection.BBA advances · 2021Article
- The Role of T Cell Receptor Signaling in the Development of Type 1 Diabetes.Frontiers in immunology · 2020Review
- Article
- Interleukin-18 Expression Increases in the Aorta and Plasma of Patients with Acute Aortic Dissection.Mediators of inflammation · 2019Article
- NLRP3 deficiency protects from type 1 diabetes through the regulation of chemotaxis into the pancreatic islets.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Increased expression of IL-18 in the serum and islets of type 1 diabetics.Molecular immunology · 2015Article
- IL-18 in inflammatory and autoimmune disease.Cellular and molecular life sciences : CMLS · 2013Review
- The immunobiology of apotransferrin in type 1 diabetes.Clinical and experimental immunology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
IL-18 has a well-established role in pro-inflammatory responses in the islets in type 1 diabetes. Here, we identify a distinctive role for IL-18 in expanding pathogenic T cells in the periphery of NOD mice. Well in advance of disease onset, the periphery of IL-18-deficient mice exhibits reduced T cell turnover, an increased prevalence of naïve and quiescent T cells, emergence of fewer effector T cells, and disease protection. Islet-reactive T cells fail to become activated in the lymphoid organs of mice lacking IL-18 and their rapid expansion is inhibited. IL-18 secretion by antigen presenting cells increases with advancing disease and is required for expression of its receptor on T cells. Our results demonstrate that induction of the IL-18 receptor reflects a critical stage of autoreactive T cell activation and expansion on the pathway toward effector T cell differentiation. This study therefore assigns a novel role to IL-18 for expanding the pool of islet-destructive T cells during pre-diabetes. This report highlights a new basic mechanism in type 1 diabetes pathogenesis and suggests that targeting the IL-18 pathway should be explored as a potential treatment strategy.
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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.