Gene expression of CD11b+ and CD8+ spleen dendritic cells from NOD and B6 mice after in vivo CpG or PBS stimulation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE75883 | GEO | 2016/02/01
SECONDARY ACCESSION(S): PRJNA305608
REPOSITORIES: GEO
Similar Datasets
Project description:The NOD (nonobese diabetic) mouse strain develops a characteristic autoimmune syndrome that closely resembles human type I diabetes. It has been suggested that NOD mice exhibit both numerical deficiency in CD4+CD25+ regulatory T cells (Treg) and reduced suppressive activity. We compared sorted CD4+CD25+ Tregs from the spleens of 6-7 week-old female NOD and nondiabetic B6.H2g7 mice. Tregs were 93±2% and 95±1% Foxp3+ in NOD and B6.H2g7 cells, respectively, on post-sort reanalysis. "Conventional" CD4+CD25- T cells (Tconv) are included as reference populations. Surprisingly, Treg "signature" is similar between the two strains, with only a few probesets that subtly deviate. Keywords: Cell population comparison from two mouse strains.
2008-12-19 | GSE6813 | GEO
Project description:NOD mice are an inbred strain that display enhanced MZ B cell differentiation from an early age. Interestingly, several lines of evidence implicate MZ B cells in this strain as important contributors to the T cell mediated beta cell destruction associated with the development of type 1 diabetes (T1D). In order to develop a better understanding of the underlying causes for augmented MZ B cell production in NOD mice, we obtained the transcriptional profiles of FO and MZ subsets and TR precursors from NOD mice and compared them to those of the B6 strain.
2013-05-16 | GSE43396 | GEO
Project description:The NOD (nonobese diabetic) mouse strain develops a characteristic autoimmune syndrome that closely resembles human type I diabetes. It has been suggested that NOD mice exhibit both numerical deficiency in CD4+CD25+ regulatory T cells (Treg) and reduced suppressive activity. We compared sorted CD4+CD25+ Tregs from the spleens of 6-7 week-old female NOD and nondiabetic B6.H2g7 mice. Tregs were 93±2% and 95±1% Foxp3+ in NOD and B6.H2g7 cells, respectively, on post-sort reanalysis. "Conventional" CD4+CD25- T cells (Tconv) are included as reference populations. Surprisingly, Treg "signature" is similar between the two strains, with only a few probesets that subtly deviate. Keywords: Cell population comparison from two mouse strains. For each strain (NOD and B6.g7), we analyzed two populations: CD4+CD25+ Treg and CD4+CD25- Tconv cells, for a total of four distinct populations. RNA from three mice were pooled for each replicate; there are three independent replicates for each population. After RMA normalization, intensity values were averaged across the three replicates and analyzed. We calculated the ratio of Treg/Tconv intensity values for each strain and compared the results.
2008-12-19 | E-GEOD-6813 | biostudies-arrayexpress
Project description:NOD mice are an inbred strain that display enhanced MZ B cell differentiation from an early age. Interestingly, several lines of evidence implicate MZ B cells in this strain as important contributors to the T cell mediated beta cell destruction associated with the development of type 1 diabetes (T1D). In order to develop a better understanding of the underlying causes for augmented MZ B cell production in NOD mice, we obtained the transcriptional profiles of FO and MZ subsets and TR precursors from NOD mice and compared them to those of the B6 strain. Red cell depleted splenocyte suspensions from from eight pooled NOD or B6 mice were stained with biotinylated anti-CD3ε (145-2C11) and CD11b (M1/70, BD Biosciences) antibodies followed by anti-biotin Microbeads (Miltenyi Biotec, Bergisch Gladbach, Germany). Separation of unlabeled B cells from samples was achieved to a >93% purity (as determined by flow cytometry) by negative depletion with an autoMACS cell sorter (Miltenyi Biotec). These cells were then stained with a cocktail of: non-stimulatory Affinipure goat anti-mouse-IgM-FITC Fab fragments from Jackson Immunoresearch; anti-CD21/35-PE (7G6), anti-CD24-biotin (30-F1; with streptavidin-PerCP secondary), B220-APC-Cy7 (RA36B2) from BD Biosciences; anti-CD93-APC (AA4.1), anti-CD23-PE-Cy7 (B3B4) from eBiosciences. T1, T2FO, T3, FO, T2MZ and MZ subsets were then separated with a FACSAria Cell Sorter (BD Biosciences). This process was repeated in an independent experiment in order to generate a duplicate sample of each B cell subset from NOD and B6 mice. Labelled cRNA from B cell samples were hybridized to Mouse Genome 430 2.0 Arrays.
2013-05-16 | E-GEOD-43396 | biostudies-arrayexpress
Project description:The aim of this study was to quantify the impact of NOD genetic vatiation on thymic negative selection transcriptional programs. Pre-selected BDC2.5 TCR Tg DP thymocytes from non-selecting B6 and NOD.H2b backgrounds were purified (Dynal CD8 FlowComp), mixed in a 1:1 ratio and stimulated with BDC mimotope-loaded TCRa-/-/NOD splenocytes for indicated periods of time and double sorted by FACS as Thy1.2+Dump-CD4+CD8+; Dump includes CD19, Gr1, CD11b, CD11c, CD49b. Following cell sorting into trizol, RNA was purified, labeled and hybridized to Affymetrix arrays. experiment type: unstimulated versus stimulated BDC/B6.Rag-/- and BDC/NOD.H2b.Rag-/- DP thymocytes
2012-01-10 | E-GEOD-34934 | biostudies-arrayexpress
Project description:The aim of this study was to quantify the impact of chimeric Foxp3-GFP protein on the Treg cell transcriptional program. Duplicate samples of Tconv (CD3+CD4+GFP-) and Treg (CD3+CD4+GFP+) splenocytes were double-sorted to achieve > 99.0% purity, from 6 weeks old male Foxp3-Fusion-GFP and Foxp3-ires-GFP mice of both B6 and NOD backgrounds. Following cell sorting into Trizol, RNA was purified, labeled and hybridized to Affymetrix arrays.
2012-04-26 | E-GEOD-37605 | biostudies-arrayexpress
Project description:Gene profiling of scramble, ACLY, and p300 KD astrocytes during NOD-EAE in B6 mice.
2024-03-21 | GSE252498 | GEO
Project description:CD11b+ CD11c- cells were isolated by cell sorting from the spleens of NOD and NOD.Idd3 mice. Cells were then either unstimulated or stimulated with peptidoglycan (5ug/ml) for 4 hours at 37 degrees prior to RNA extraction. Peptidoglycan was chosen as a stimulus due to its know ability to stimulate CD11b+ cells through Toll-like receptor 2 and our previous data showing biological differences between NOD and NOD.Idd3-derived CD11b+CD11c- cells after stimulation with peptidoglycan. CD11b+ cells from NOD and NOD.Idd3 were either unstimulated or stimulated with peptidoglycan(PGN) for 4 hours at 37 degerees prior to RNA extraction.
2010-09-28 | E-GEOD-24350 | biostudies-arrayexpress
Project description:CD11b+ CD11c- cells were isolated by cell sorting from the spleens of NOD and NOD.Idd3 mice. Cells were then either unstimulated or stimulated with peptidoglycan (5ug/ml) for 4 hours at 37 degrees prior to RNA extraction. Peptidoglycan was chosen as a stimulus due to its know ability to stimulate CD11b+ cells through Toll-like receptor 2 and our previous data showing biological differences between NOD and NOD.Idd3-derived CD11b+CD11c- cells after stimulation with peptidoglycan.
2010-09-28 | GSE24350 | GEO
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
2005-04-14 | GSE2524 | GEO