ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- GAD vaccine reduces insulin loss in recently diagnosed type 1 diabetes: findings from a Bayesian meta-analysis.Diabetologia · 2017Pooled it
- 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
- Increased autoimmune diabetes in pIgR-deficient NOD mice is due to a "Hitchhiking" interval that refines the genetic effect of Idd5.4.PloS one · 2015Article
- Cytoplasmic poly(A) binding protein C4 serves a critical role in erythroid differentiation.Molecular and cellular biology · 2014Article
- Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.PloS one · 2014Article
- 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
- Article
- Cellular mechanisms of restored β-cell tolerance mediated by protective alleles of Idd3 and Idd5.Diabetes · 2012Article
- Identification of the Mhc region as an asthma susceptibility locus in recombinant congenic mice.American journal of respiratory cell and molecular biology · 2011Article
- Evidence that Cd101 is an autoimmune diabetes gene in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Advances and challenges in biomarker development for type 1 diabetes prediction and prevention using omic technologies.Expert opinion on medical diagnostics · 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
- Genetic and Molecular Basis of QTL of Diabetes in Mouse: Genes and Polymorphisms.Current genomics · 2008Article
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Authors and funding
8 authors at 3 institutions in 4 countries.
Funding
Abstract
NOD.Idd3/5 congenic mice have insulin-dependent diabetes (Idd) regions on chromosomes 1 (Idd5) and 3 (Idd3) derived from the nondiabetic strains B10 and B6, respectively. NOD.Idd3/5 mice are almost completely protected from type 1 diabetes (T1D) but the genes within Idd3 and Idd5 responsible for the disease-altering phenotype have been only partially characterized. To test the hypothesis that candidate Idd genes can be identified by differential gene expression between activated CD4+ T cells from the diabetes-susceptible NOD strain and the diabetes-resistant NOD.Idd3/5 congenic strain, genome-wide microarray expression analysis was performed using an empirical Bayes method. Remarkably, 16 of the 20 most differentially expressed genes were located in the introgressed regions on chromosomes 1 and 3, validating our initial hypothesis. The two genes with the greatest differential RNA expression on chromosome 1 were those encoding decay-accelerating factor (DAF, also known as CD55) and acyl-coenzyme A dehydrogenase, long chain, which are located in the Idd5.4 and Idd5.3 regions, respectively. Neither gene has been implicated previously in the pathogenesis of T1D. In the case of DAF, differential expression of mRNA was extended to the protein level; NOD CD4+ T cells expressed higher levels of cell surface DAF compared with NOD.Idd3/5 CD4+ T cells following activation with anti-CD3 and -CD28. DAF up-regulation was IL-4 dependent and blocked under Th1 conditions. These results validate the approach of using congenic mice together with genome-wide analysis of tissue-specific gene expression to identify novel candidate genes in T1D.
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