ArticleDiabetes2010
Idd9.2 and Idd9.3 protective alleles function in CD4+ T-cells and nonlymphoid cells to prevent expansion of pathogenic islet-specific CD8+ T-cells.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- PD-1 expressing islet-specific CD4Immunology and cell biology · 2025Article
- Islet-specific CD8Immunology and cell biology · 2023Article
- Regulatory T Cells Induced by Single-Peptide Liposome Immunotherapy Suppress Islet-Specific T Cell Responses to Multiple Antigens and Protect from Autoimmune Diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Genetic Variation in Type 1 Diabetes Reconfigures the 3D Chromatin Organization of T Cells and Alters Gene Expression.Immunity · 2020Article
- Integrative QTL analysis of gene expression and chromatin accessibility identifies multi-tissue patterns of genetic regulation.PLoS genetics · 2020Article
- The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Frontiers in endocrinology · 2018Article
- CD11a/ICAM-1 blockade combined with IL-2 targeting therapy causes a paradoxical acceleration of type 1 diabetes.Immunology and cell biology · 2017Article
- Congenic mapping identifies a novel Idd9 subregion regulating type 1 diabetes in NOD mice.Immunogenetics · 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
- Genome-wide transcriptional analyses of islet-specific CD4+ T cells identify Idd9 genes controlling diabetogenic T cell function.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.PloS one · 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
- 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
- Cellular mechanisms of restored β-cell tolerance mediated by protective alleles of Idd3 and Idd5.Diabetes · 2012Article
- Article
- Use of nonobese diabetic mice to understand human type 1 diabetes.Endocrinology and metabolism clinics of North America · 2010Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveMultiple type 1 diabetes susceptibility genes have now been identified in both humans and mice, yet mechanistic understanding of how they impact disease pathogenesis is still minimal. We have sought to dissect the cellular basis for how the highly protective mouse Idd9 region limits the expansion of autoreactive CD8(+) T-cells, a key cell type in destruction of the islets. RESEARCH DESIGN AND
methodsWe assess the endogenous CD8(+) T-cell repertoire for reactivity to the islet antigen glucose-6-phosphatase-related protein (IGRP). Through the use of adoptively transferred T-cells, bone marrow chimeras, and reconstituted severe combined immunodeficient mice, we identify the protective cell types involved.
resultsIGRP-specific CD8(+) T-cells are present at low frequency in the insulitic lesions of Idd9 mice and could not be recalled in the periphery by viral expansion. We show that Idd9 genes act extrinsically to the CD8(+) T-cell to prevent the massive expansion of pathogenic effectors near the time of disease onset that occurs in NOD mice. The subregions Idd9.2 and Idd9.3 mediated this effect. Interestingly, the Idd9.1 region, which provides significant protection from disease, did not prevent the expansion of autoreactive CD8(+) T-cells. Expression of Idd9 genes was required by both CD4(+) T-cells and a nonlymphoid cell to induce optimal tolerance.
conclusionsIdd9 protective alleles are associated with reduced expansion of IGRP-specific CD8(+) T-cells. Intrinsic expression of protective Idd9 alleles in CD4(+) T-cells and nonlymphoid cells is required to achieve an optimal level of tolerance. Protective alleles in the Idd9.2 congenic subregion are required for the maximal reduction of islet-specific CD8(+) T-cells.
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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.