Expression data from NOD and B10 CD4 splenocytes
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE36550 | GEO | 2019/09/23
REPOSITORIES: GEO
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Project description:Because activation of the immune response is dependent on extensive changes in gene expression, it is likely that a major component of inter-individual variation in the immune response is ultimately mediated at the level of gene regulation. Here, we examine the influence of genetic variation on inducible gene expression in the murine immune response. We extracted primary CD4 splenocytes from inbred strains A/J, C57BL/6J, BALB/c, DBA/2J, and 129x1/SvJ (3 animals/strain) and measured mRNA transcript levels using microarrays in both basal state and four hours after stimulation with PMA/Ionomycin. We report strain-specific genome-wide differences in mRNA expression between A/J, Balb/c, C57BL/6J, DBA/2J and 129X1/SvJ inbred mice in CD4 splenocytes in basal, stimulated (4hr, PMA/I) states.
2019-09-23 | GSE36551 | GEO
Project description:During the course of infection, T cells are confronted with a multitude of non self epitopes but only respond to a few epitopes and neglect other potentially immunogenic peptides. Restriction of T cell responses to a small number of selected epitopes (immunodominance) is a central feature of immune responses. Immunodominance is considered to be disadvantageous to the host because it allows pathogens to escape by selectively mutating the relevant epitope(s). Using Affymetrix microarrays, we compared the gene expression profile of unprimed CD8 T cells to that of effector CD8 T cells specific for a dominant (H7a) and a nondominant (HY) Ag. Our key finding is that T cells specific for the dominant and nondominant Ags displayed similar gene expression profiles except for a few gene transcripts, such as Gzma, Sell, Il7r and Klrg1, that contribute to the fitness of effector CD8 T cells. The differences between HY- and H7a-specific CD8 T cells were validated by real-time PCR and flow cytometry analyses. We propose that, by leading to selective expansion of the fittest CD8 effector T cells, immunodominance may be beneficial to the host. Inhibition of T cell response to nondominant Ags would ensure that host resources (APCs, cytokines) for which T cells compete are devoted to T cells that have the best effector potential. One implication is that, in general, favouring expansion of the fittest effector T cells may be more important that increasing the diversity of the T cell repertoire. Experiment Overall Design: B10.H7b female mice were primed by i.p. injection of a cell mixture containing 2 x 107 B10 male splenocytes and 2 x 107 B10.H7b male splenocytes. On day 14 after priming, splenocytes were labeled with anti-CD8 Ab as well as H7a- and HY-Tet labeled with different fluorochromes. Then, three populations of splenocytes were purified using a FACS cell sorting: HYTet+ (n=4), H7aTet+ (n=4), and Tet- (n=5) CD8 T cells. RNA of sorted T cells was extracted and linearly amplified, cRNA was prepared, and Affymetrix Mouse Genome 430 2.0 oligonucleotide arrays were used to analyze gene expression.
2008-06-12 | E-GEOD-2924 | biostudies-arrayexpress
Project description:Divergence has occured between the B10.BR-H2k H2-T18a/SgSnJJrep and B10.BR-H2k H2-T18a/SgSnJ (drifted) mouse strains, resulting in altered antigenic recognition and differential bone marrow engraftment capability. The microarray data demonstrate that the transcriptional profile of genes associated with hematopoiesis differs between lineage negative (as a marker for hematopoietic stem cells) bone marrow cells isolated from the B10.BR-H2k H2-T18a/SgSnJJrep and B10.BR-H2k H2-T18a/SgSnJ (drifted) mouse strains.
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Project description:we used genome-wide transcriptome analysis to profile the mRNA, long noncoding RNA (lncRNA), and microRNA (miRNA) expression of B10 cells, an antigen-specific Cd1dhiCd5+Cd19hiIl10 competent regulatory B cell. Potential key upstream regulators (including transcription factors, cytokines, trans-membrane receptors, and kinases) for Breg biogenesis and function were identified. B10+ B cells (Cd1dhiCd5+Cd19hiIl10+) and B10- cells (Cd1d-Cd5-Cd19hiIl10-) from mouse splenic B cell were sorted for RNA preparation. Two independent repeats were prepared for microarray analysis
2015-10-29 | E-GEOD-63374 | biostudies-arrayexpress
Project description:we used genome-wide transcriptome analysis to profile the mRNA, long noncoding RNA (lncRNA), and microRNA (miRNA) expression of B10 cells, an antigen-specific Cd1dhiCd5+Cd19hiIl10 competent regulatory B cell. Potential key upstream regulators (including transcription factors, cytokines, trans-membrane receptors, and kinases) for Breg biogenesis and function were identified. B10+ B cells (Cd1dhiCd5+Cd19hiIl10+) and B10- cells (Cd1d-Cd5-Cd19hiIl10-) from mouse splenic B cell were sorted for RNA preparation. Two independent repeats were prepared for RNA-seq
2015-10-29 | E-GEOD-63426 | biostudies-arrayexpress
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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Project description:Divergence has occured between the B10.BR-H2k H2-T18a/SgSnJJrep and B10.BR-H2k H2-T18a/SgSnJ (drifted) mouse strains, resulting in altered antigenic recognition and differential bone marrow engraftment capability. The microarray data demonstrate that the transcriptional profile of genes associated with hematopoiesis differs between lineage negative (as a marker for hematopoietic stem cells) bone marrow cells isolated from the B10.BR-H2k H2-T18a/SgSnJJrep and B10.BR-H2k H2-T18a/SgSnJ (drifted) mouse strains. Bone marrow cells from ten male mice of each strain, aged 10-12 weeks, were harvested. One pooled sample was analyzed for each strain.
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