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Comparison of gene expression profiles in NOD and Idd9 CD4+ T cells

ABSTRACT: Nonobese diabetic (NOD) mice congenic for B10 derived genes in the Idd9 region of chromosome 4 are highly protected from the development of diabetes. In order to identify possible candidate genes within the Idd9 susceptibility region and possible downstream mediators of protection, we compared gene expression between NOD and Idd9 CD4+ T-cells. CD4+ T-cells with an activated phenotype (CD44-high/CD62L-low) were sorted from the pancreatic lymph nodes of female 8-week old mice. Mice were bred at Taconic farms and were line 905 (NOD.B10-Idd9 congenic) and line 6359 (NOD-like control strain with a B10 congenic region on chromosome 1 which does not modify diabetes incidence). Three replicate samples were prepared, each from four pooled pancreatic lymph nodes. CD4+CD44-highCD62L-low T-cells were sorted from each sample.

ORGANISM(S): Mus musculus

SUBMITTER: Steven Head

PROVIDER: E-GEOD-35482 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Comparison of gene expression profiles in NOD and Idd9 CD4+ T cells

Project description:Nonobese diabetic (NOD) mice congenic for B10 derived genes in the Idd9 region of chromosome 4 are highly protected from the development of diabetes. In order to identify possible candidate genes within the Idd9 susceptibility region and possible downstream mediators of protection, we compared gene expression between NOD and Idd9 CD4+ T-cells. CD4+ T-cells with an activated phenotype (CD44-high/CD62L-low) were sorted from the pancreatic lymph nodes of female 8-week old mice.

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Project description:Transcriptional response of murine allogeneic T cells (B10.BR) after; stimulation with different organ-derived (spleen, liver, peripheral and; mesenteric lymph nodes) dendritic cells (C57BL/6) in vitro Experiment Overall Design: We stimulated B10.BR T cells with dendritic cells derived from different C57BL/6 organs for four days and then performed array experiments on the T cells.

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Project description:Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta-cell destruction. It is a complex genetic trait driven by over 30 genetic loci with parallels between humans and mice. The NOD mouse spontaneously develops autoimmune diabetes and is widely used to identify insulin-dependent diabetes (Idd) genetic loci linked to diabetes susceptibility. While many Idd loci have been extensively studied, the impact of the Idd2 locus on autoimmune diabetes susceptibility remains to be defined. To address this, we generated a NOD congenic mouse bearing B10 resistance alleles on chromosome 9 in a locus coinciding with part of the Idd2 locus and find that NOD.B10-Idd2 congenic mice are highly resistant to diabetes. Bone marrow chimera and adoptive transfer experiments show that the B10 protective alleles provide resistance in an immune cell-intrinsic manner. While no T cell-intrinsic differences between NOD and NOD.B10-Idd2 mice were observed, we find that the Idd2 resistance alleles limit the formation of spontaneous and induced germinal centers. Comparison of the B cell transcriptome profile from NOD and NOD.B10-Idd2 mice reveal that resistance alleles at the Idd2 locus affect the expression of specific MHC molecules, a result confirmed by flow cytometry. Altogether, these data demonstrate that resistance alleles at the Idd2 locus impair germinal center formation and influence MHC expression, both of which likely contribute to reduce diabetes incidence.

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