Project description:Functional liability conferred by gene expression profile can be a possible basis for diseases phenotype. By comparing gene expression profiles in splenic T cells from NOD, C57BL/6 mice and their congenic strains with altered MHCs (NOD.H2^h4 , B6.NOD/Idd1,5/), we identified that the NOD splenic T cells have a strain dependent, tissue specific unique gene expression profile that can be but not necessarily be modulated by alternation of MHC. The NOD splenic T cells gene expression profile indicated a deregulated stress response system, especially heat shock protein family. We demonstrated that NOD splenic T cells have apoptosis defect in vivo and in vitro. Therefore, the gene expression profile may confer liability upon NOD splenic T cells to make them more susceptible to apoptosis, which can be a critical factor to lead to NOD lymphopenia. As recently described, compensatory homeostatic proliferation, driven by lymphopenia, generates autoimmunity in the NOD mouse. Keywords: other
Project description:Comparison of temporal small RNA gene expression from Mus musculus blood. The RNA-seq data comprise 5 groups at ages: 2, 9, 15, 24 and 30 months. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
Project description:Comparison of temporal small RNA gene expression from Mus musculus skin. The RNA-seq data comprise 5 groups at ages: 2, 9, 15, 24 and 30 months. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
Project description:Functional liability conferred by gene expression profile can be a possible basis for diseases phenotype. By comparing gene expression profiles in splenic T cells from NOD, C57BL/6 mice and their congenic strains with altered MHCs (NOD.H2^h4 , B6.NOD/Idd1,5/), we identified that the NOD splenic T cells have a strain dependent, tissue specific unique gene expression profile that can be but not necessarily be modulated by alternation of MHC. The NOD splenic T cells gene expression profile indicated a deregulated stress response system, especially heat shock protein family. We demonstrated that NOD splenic T cells have apoptosis defect in vivo and in vitro. Therefore, the gene expression profile may confer liability upon NOD splenic T cells to make them more susceptible to apoptosis, which can be a critical factor to lead to NOD lymphopenia. As recently described, compensatory homeostatic proliferation, driven by lymphopenia, generates autoimmunity in the NOD mouse.
Project description:Comparison of temporal small RNA gene expression from Mus musculus right hemisphere. The RNA-seq data comprise 5 groups at ages: 2, 9, 15, 24 and 30 months. Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
