ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Expression of diabetes-associated genes by dendritic cells and CD4 T cells drives the loss of tolerance in nonobese diabetic mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Altered Function of Antigen-Presenting Cells in Type 1 Diabetes: A Challenge for Antigen-Specific Immunotherapy?Diabetes · 2018Review
- A NovelJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- APC-targeted proinsulin expression inactivates insulin-specific memory CD8Immunology and cell biology · 2017Article
- Reduced interleukin-2 responsiveness impairs the ability of Treg cells to compete for IL-2 in nonobese diabetic mice.Immunology and cell biology · 2016Article
- The Role of Dendritic Cell Subsets and Innate Immunity in the Pathogenesis of Type 1 Diabetes and Other Autoimmune Diseases.Frontiers in immunology · 2015Review
- Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.PloS one · 2014Article
- Self-antigen presentation by dendritic cells in autoimmunity.Frontiers in immunology · 2014Review
- Dendritic cell subsets in type 1 diabetes: friend or foe?Frontiers in immunology · 2013Review
- 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
- Extrathymic Aire-expressing cells are a distinct bone marrow-derived population that induce functional inactivation of CD4⁺ T cells.Immunity · 2013Article
- Genetic interactions among Idd3, Idd5.1, Idd5.2, and Idd5.3 protective loci in the nonobese diabetic mouse model of type 1 diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- The B10 Idd9.3 locus mediates accumulation of functionally superior CD137(+) regulatory T cells in the nonobese diabetic type 1 diabetes model.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Subcongenic analyses reveal complex interactions between distal chromosome 4 genes controlling diabetogenic B cells and CD4 T cells in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Cellular mechanisms of restored β-cell tolerance mediated by protective alleles of Idd3 and Idd5.Diabetes · 2012Article
- Identification of Cd101 as a susceptibility gene for Novosphingobium aromaticivorans-induced liver autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Reduced IL-2 expression in NOD mice leads to a temporal increase in CD62Llo FoxP3+ CD4+ T cells with limited suppressor activity.European journal of immunology · 2011Article
- Interleukin-2 inhibits FMS-like tyrosine kinase 3 receptor ligand (flt3L)-dependent development and function of conventional and plasmacytoid dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Self-antigen presentation by dendritic cells and lymphoid stroma and its implications for autoimmunity.Current opinion in immunology · 2011Review
- Article
- Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.Seminars in immunopathology · 2011Review
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Authors and funding
12 authors at 7 institutions in 5 countries.
Funding
Abstract
In humans and NOD mice, defects in immune tolerance result in the spontaneous development of type-1-diabetes. Recent studies have ascribed a breakdown in tolerance to dysfunction in regulatory T cells that is secondary to reduced IL-2 production by T cells having the NOD diabetes susceptibility region insulin-dependent diabetes 3 (Idd3). In this study, we demonstrate a peripheral tolerance defect in the dendritic cells of NOD mice that is independent of regulatory T cells. NOD CD8 T cells specific for islet Ags fail to undergo deletion in the pancreatic lymph nodes. Deletion was promoted by expression of the protective alleles of both Idd3 (Il2) and Idd5 in dendritic cells. We further identify a second tolerance defect that involves endogenous CD4 T cell expression of the disease-promoting NOD alleles of these genetic regions. Pervasive insulitis can be reduced by expression of the Idd3 and Idd5 protective alleles by either the Ag-presenting cell or lymphocytes.
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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.