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RNA-sequencing of CD4+ T cells isolated from C57BL/6 and B6.NZMSle1/Sle2/Sle3 treated with ant-CD45RB

ABSTRACT: RNA-sequencing of CD4+ T cells isolated from C57BL/6 and B6.NZMSle1/Sle2/Sle3 treated with ant-CD45RB

PROVIDER: PRJNA753519 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15409707_1.fastq.gz	Fastqsanger.gz
	SRR15409707_2.fastq.gz	Fastqsanger.gz
	SRR15409708_1.fastq.gz	Fastqsanger.gz
	SRR15409708_2.fastq.gz	Fastqsanger.gz
	SRR15409709_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing of CD4+ T cells isolated from C57BL/6 and B6.NZMSle1/Sle2/Sle3 treated with ant-CD45RB

Project description:C57BL/6 or B6.NZMSle1/Sle2/Sle3 were treated with 100ug of anti-CD45RB (MB23G2) on days 0,1,3,5,and 7. Mice were sacrificied and spleens were harvested and sorted for untouched CD4+ T cells using negative Magentic-activated cell sorting. RNA was isolated and the subjected to RNA sequencing.

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Splenic CD4 T cells in naïve C57BL/6 mice or during Plasmodium berghei ANKA infection in C57BL/6 and B6.GzmB-/- mice.

Project description:Infection of C57BL/6 mice with Plasmodium berghei ANKA (PbA) is a well-established experimental model of cerebral malaria (ECM). ECM is characterised by high levels of parasite sequestration and recruitment of pathogenic CD8+ T cells to the brain. The role of CD4+ T cells in this model has not yet been fully elucidated, although our laboratory has recently shown that CD4+ T cell depletion prior to infection results in significantly lower parasite burdens and protection from ECM. These data highlight a pathogenic role for CD4+ T cells in ECM. Our unpublished observations indicate that mice lacking the CD8+ T cell cytolytic effector molecule, Granzyme B, (GzmB), are resistant to ECM, showing markedly reduced parasite burdens. Late depletion of CD4+ T cells from PbA-infected GzmB-deficient mice results in enhanced parasite burdens, indicating that these cells may play an anti-parasitic role. In the present study, we have analysed splenic CD4+ T cell gene expression profiles in naïve C57BL/6 mice, and PbA-infected wild-type and GzmB-deficent mice to further our understanding of the CD4+ T cell response in ECM. Splenic CD4 T cells isolated by cell sorting from either uninfected C57BL/6 or PbA-infected C57BL/6 or B6.GzmB-/- mice at day 4 post-infection. Total RNA obtained from four mice per group.

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Gene expression data from teratomas formed by C57BL/6 (B6) ES and EiPS cells in B6 mice

Project description:Embryonic fibroblast from C57BL/6 (B6) mice were reprogrammed to EiPS without exogenous DNA integration using an single episomal vector. The EiPS cells and B6 ES cells were then transplanted into B6 mice to form teratomas. We used microarrays to profile the gene expression differences between the teratomas formed by B6 ES cells and EiPS cells.

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Project description:Sle1c is a sublocus of the NZM2410-derived Sle1 major susceptibility locus. We have previously shown that Sle1c contributes to lupus pathogenesis by conferring CD4+ T cell-intrinsic hyperactivation and increased susceptibility to chronic graft-versus-host disease (cGVHD) that mapped to the centromeric portion of the locus. In this study, we have refined the centromeric sublocus to a 675Kb interval, termed Sle1c2. Recombinant congenic strains expressing Sle1c2 exhibited a T cell-intrinsic CD4+ T cell hyperactivation and cGVHD susceptibility, similar to mice with the parental Sle1c. We performed a microarray analysis on CD4+ T cells to gain insights into the transcriptional programs that regulate the hyperactivation conferred by Sle1c2. CD4+ T cell cDNA was prepared from spenocytes from 5 mice from each strain and B6.Sle1c2 gene expression was compared to B6 gene expresion.

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Mus musculus strain:C57BL/6J (B6)

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Gene expression profiles of CD4+CD25+ Tregs from NOD and B6.H2g7 mice

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.

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