ArticleJournal of immunology (Baltimore, Md. : 1950)2006
Genes within the Idd5 and Idd9/11 diabetes susceptibility loci affect the pathogenic activity of B cells in nonobese diabetic mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Frontiers in endocrinology · 2018Article
- Genetic and Small Molecule Disruption of the AID/RAD51 Axis Similarly Protects Nonobese Diabetic Mice from Type 1 Diabetes through Expansion of Regulatory B Lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Development of the Nonobese Diabetic Mouse and Contribution of Animal Models for Understanding Type 1 Diabetes.Pancreas · 2017Review
- B Cell Receptor Affinity for Insulin Dictates Autoantigen Acquisition and B Cell Functionality in Autoimmune Diabetes.Journal of clinical medicine · 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
- 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
- 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
- Comparative genetics: synergizing human and NOD mouse studies for identifying genetic causation of type 1 diabetes.The review of diabetic studies : RDS · 2012Review
- Loss of intra-islet CD20 expression may complicate efficacy of B-cell-directed type 1 diabetes therapies.Diabetes · 2011Article
- B cell depletion in autoimmune diabetes: insights from murine models.Expert opinion on therapeutic targets · 2011Review
- Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.Seminars in immunopathology · 2011Review
- Article
- Idd9.1 locus controls the suppressive activity of FoxP3+CD4+CD25+ regulatory T-cells.Diabetes · 2010Article
- Expression of diabetes-associated genes by dendritic cells and CD4 T cells drives the loss of tolerance in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Change you can B(cell)eive in: recent progress confirms a critical role for B cells in type 1 diabetes.Current opinion in endocrinology, diabetes, and obesity · 2009Review
- Idd9/11 genetic locus regulates diabetogenic activity of CD4 T-cells in nonobese diabetic (NOD) mice.Diabetes · 2008Article
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Autoreactive T cells clearly mediate the pancreatic beta cell destruction causing type 1 diabetes (T1D). However, studies in NOD mice indicate that B cells also contribute to pathogenesis because their ablation by introduction of an Igmunull mutation elicits T1D resistance. T1D susceptibility is restored in NOD.Igmunull mice that are irradiated and reconstituted with syngeneic bone marrow plus NOD B cells, but not syngeneic bone marrow alone. Thus, we hypothesized some non-MHC T1D susceptibility (Idd) genes contribute to disease by allowing development of pathogenic B cells. Supporting this hypothesis was the finding that unlike those from NOD donors, engraftment with B cells from H2g7 MHC-matched, but T1D-resistant, nonobese-resistant (NOR) mice failed to restore full disease susceptibility in NOD.Igmunull recipients. T1D resistance in NOR mice is mainly encoded within the Idd13, Idd5.2, and Idd9/11 loci. B cells from NOD congenic stocks containing Idd9/11 or Idd5.1/5.2-resistance loci, respectively, derived from the NOR or C57BL/10 strains were characterized by suppressed diabetogenic activity. Immature autoreactive B cells in NOD mice have an impaired ability to be rendered anergic upon Ag engagement. Interestingly, both Idd5.1/5.2 and Idd9/11-resistance loci were found to normalize this B cell tolerogenic process, which may represent a mechanism contributing to the inhibition of T1D.
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