ArticleBiology direct2007
Resistance of the target islet tissue to autoimmune destruction contributes to genetic susceptibility in Type 1 diabetes.
Article in Biology direct, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Untangling the genetics of beta cell dysfunction and death in type 1 diabetes.Molecular metabolism · 2024Review
- The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Frontiers in endocrinology · 2018Article
- The Type 1 Diabetes-Resistance LocusJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Novel role for matricellular proteins in the regulation of islet β cell survival: the effect of SPARC on survival, proliferation, and signaling.The Journal of biological chemistry · 2014Article
- Fine mapping of type 1 diabetes regions Idd9.1 and Idd9.2 reveals genetic complexity.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Article
- Predicting disease-related subnetworks for type 1 diabetes using a new network activity score.Omics : a journal of integrative biology · 2012Article
- IL-18 is required for self-reactive T cell expansion in NOD mice.Journal of autoimmunity · 2011Article
- Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.Seminars in immunopathology · 2011Review
- Antigen-Experienced CD4lo T Cells Are Linked to Deficient Contraction of the Immune Response in Autoimmune Diabetes.Autoimmune diseases · 2010Article
- Article
- Idd9.1 locus controls the suppressive activity of FoxP3+CD4+CD25+ regulatory T-cells.Diabetes · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledType 1 diabetes occurs when self-reactive T lymphocytes destroy the insulin-producing islet beta cells of the pancreas. The defects causing this disease have often been assumed to occur exclusively in the immune system. We present evidence that genetic variation at the Idd9 diabetes susceptibility locus determines the resilience of the targets of autoimmunity, the islets, to destruction. Susceptible islets exhibit hyper-responsiveness to inflammatory cytokines resulting in enhanced cell death and increased expression of the death receptor Fas. Fas upregulation in beta cells is mediated by TNFR2, and colocalization of TNFR2 with the adaptor TRAF2 in NOD beta cells is altered. TNFR2 lies within the candidate Idd9 interval and the diabetes-associated variant contains a mutation adjacent to the TRAF2 binding site. A component of diabetes susceptibility may therefore be determined by the target of the autoimmune response, and protective TNFR2 signaling in islets inhibit early cytokine-induced damage required for the development of destructive autoimmunity. REVIEWERS: This article was reviewed by Matthiasvon Herrath, HaraldVon Boehmer, and Ciriaco Piccirillo (nominated by Ethan Shevach).
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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.