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ScRNA-seq analyses on Thy1.1+Thy1.2+ MDR1-sufficient and Thy1.1+Thy1.2- MDR1-deficient P14 CD8+ T cells from ten congenically-transferred and LCMV-infected wild type B6 mice at day 8 post-infection

ABSTRACT: scRNA-seq analyses on Thy1.1+Thy1.2+ MDR1-sufficient and Thy1.1+Thy1.2- MDR1-deficient P14 CD8+ T cells from ten congenically-transferred and LCMV-infected wild type B6 mice at day 8 post-infection

PROVIDER: PRJNA599079 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10829875.fastq.gz	Fastqsanger.gz
	SRR10829876.fastq.gz	Fastqsanger.gz
	SRR10829877.fastq.gz	Fastqsanger.gz
	SRR10829878.fastq.gz	Fastqsanger.gz
	SRR10829879.fastq.gz	Fastqsanger.gz

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scRNA-seq analyses on Thy1.1+Thy1.2+ MDR1-sufficient and Thy1.1+Thy1.2- MDR1-deficient P14 CD8+ T cells from ten congenically-transferred and LCMV-infected wild type B6 mice at day 8 post-infection

Project description:Multidrug resistance (MDR)-1 acts as a chemotherapeutic drug efflux pump in tumor cells, although its physiologic functions remain enigmatic. Using a recently-developed MDR1-knockin reporter allele (Abcb1aAME/+), we found that constitutive MDR1 expression amongst hematopoietic cells was observed mainly in cytolytic lymphocytes—including CD8+ cytotoxic T lymphocytes (CTL) and natural killer cells—and regulated by Runt-related (Runx) transcription factors. Although MDR1 was dispensable for naïve CD8+ T cell development, it was required for both normal accumulation of effector CTL following acute viral infection and protective function of memory CTL upon challenge with an intracellular bacterium. MDR1 acted early after naïve CD8+ T cell activation to suppress oxidative stress, enforce survival and safeguard mitochondrial function in developing CTL. Together, these data highlight an important endogenous function of MDR1 in cell-mediated immune responses, and suggest that ongoing efforts to intentionally inhibit MDR1 in cancer patients could be counter-productive.

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Expression data from LCMV-infected P14 and Akt transgenic P14 CD8 T cells

Project description:The PI3K/Akt signaling pathway impacts various aspects of CD8 T cell homeostasis, such as effect versus memory cell differentiation, during viral infection. We used microarrays to determine which downstream molecules were affected and what other signaling pathways were interconnected with the Akt pathway by constitutive activation of Akt in LCMV-infected CD8 T cells. Splenocytes from naive P14/WT or P14/Akt mice were stained with anti-CD8 and anti-Ly5.1, and CD8 T cells were sorted using a FACSAria II instrument. Purified Ly5.1+ CD8 T cells from P14/WT or P14/Akt mice were transferred into B6 mice, which were subsequently infected with LCMV Armstrong. At day 8 post infection, splenocytes were stained with anti-CD8, anti-Ly5.1, anti-KLRG1, and anti-CD127. Following staining, short-lived effector cells (SLECs) and memory precursor effector cells (MPECs) were sorted using the FACSAria II instrument; the purity of the sorted cells was >95%. A total of 5 samples were analyzed, including WT naive, WT SLEC, WT MPEC, Akt naive and Akt SLEC.

2012-03-01 | E-GEOD-36168 | biostudies-arrayexpress

RNA sequencing analysis of transferred C1qbp sufficient and deficient CD8+ T cells sorted from donor mice post infection with LCMV Armstrong

Project description:Tthis study is aimed to explore how C1qbp deficiency affects the mRNA expressing profiling during the differentiation stage of CD8+ T cells.Naïve WT and C1qbp KO P14 cells and transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 3, 5, 7 post-infection with LCMV Armstrong were collected and treated for RNA-seq. RNA-Seq analysis revealed transcriptomic changes between WT and C1qbp KO CD8+ T cells. Naïve WT and C1qbp KO CD8+ T cells showed similar gene expressing profiling. On day 3, 5, 7 post-infection with LCMV Armstrong, WT and C1qbp KO CD8+ T cells showed 341, 1,164 and 437 differentially expressed genes respectively.

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Chip-seq, ATAC-seq, and RNA-seq of murine P14 T cells WT or FOXO1 KO, responding in vivo to LCMV-ARM

Project description:P14 CD8+ murine T cells were adoptively transferred to C57BL/6 hosts and infected with LCMV-ARM. At indicated times post-infection (see sample name), P14 T cells of the indicated cell-surface phenotype were isolated and sujectected to ChIP-seq, RNA-seq or ATAC-seq.

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The Xenobiotic Transporter Mdr1 Enforces T Cell Homeostasis in the Presence of Intestinal Bile Acids

Project description:This SuperSeries is composed of the SubSeries listed below. CD4+ T cells are tightly regulated by microbiota in the intestine, but whether intestinal T cells interface with host-derived metabolites is less clear. Here, we show that CD4+ T effector (Teff) cells upregulated the xenobiotic transporter, Mdr1, in the ileum to maintain homeostasis in the presence of bile acids. Whereas wild-type Teff cells upregulated Mdr1 in the ileum, those lacking Mdr1 displayed mucosal dysfunction and induced Crohn?s disease-like ileitis following transfer into Rag1-/- hosts. Mdr1 mitigated oxidative stress and enforced homeostasis in Teff cells exposed to conjugated bile acids (CBAs), a class of liver-derived emulsifying agents that actively circulate through the ileal mucosa. Blocking ileal CBA reabsorption in transferred Rag1-/- mice restored Mdr1-deficient Teff cell homeostasis and attenuated ileitis. Further, a subset of ileal Crohn?s disease patients displayed MDR1 loss of function. Together, these results suggest that coordinated interaction between mucosal Teff cells and CBAs in the ileum regulate intestinal immune homeostasis.

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The Xenobiotic Transporter Mdr1 Enforces T Cell Homeostasis in the Presence of Intestinal Bile Acids [Rh123hi-lo RNA-Seq]

Project description:CD4+ T cells are tightly regulated by microbiota in the intestine, but whether intestinal T cells interface with host-derived metabolites is less clear. Here, we show that CD4+ T effector (Teff) cells upregulated the xenobiotic transporter, Mdr1, in the ileum to maintain homeostasis in the presence of bile acids. Whereas wild-type Teff cells upregulated Mdr1 in the ileum, those lacking Mdr1 displayed mucosal dysfunction and induced Crohn’s disease-like ileitis following transfer into Rag1-/- hosts. Mdr1 mitigated oxidative stress and enforced homeostasis in Teff cells exposed to conjugated bile acids (CBAs), a class of liver-derived emulsifying agents that actively circulate through the ileal mucosa. Blocking ileal CBA reabsorption in transferred Rag1-/- mice restored Mdr1-deficient Teff cell homeostasis and attenuated ileitis. Further, a subset of ileal Crohn’s disease patients displayed MDR1 loss of function. Together, these results suggest that coordinated interaction between mucosal Teff cells and CBAs in the ileum regulate intestinal immune homeostasis.

2020-01-10 | GSE143404 | GEO

The Xenobiotic Transporter Mdr1 Enforces T Cell Homeostasis in the Presence of Intestinal Bile Acids [shMdr1 RNA-seq in vivo]

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RNA-Seq of CD8+ T cell subsets during LCMV infection [RNA-seq_D5_JQ1]

Project description:P14 cells were transferred to naïve mice subsequently infected with LCMV. Mice were treated with JQ1 or vehicle on days 1-4 of infection. On day 5 of infection KLRG1loCD127lo EEC were sorted for RNAseq analysis. In a separate experiment, P14 cells were transduced with shBrd4a or shBrd4b and mixed with shCtrl transduced P14 cells, and then transferred into naïve mice subsequently infected with LCMV. On day 5 post-infection, transduced EEC were sorted for RNAseq.

2021-05-21 | GSE173510 | GEO

Expression profiling of MDR1+ and MDR1- human memory T cells from the blood and clinically-inflamed gut tissue

Project description:The aim of this study was to characterize the transcriptional signature of MDR1+ human memory T cells isolated from clinically inflamed gut tissue, and compare it to local MDR1- memory T cells Human mononuclear cells were isolated from the peripheral blood of a healthy adult donor (Ficol density centrifugation) or from resected lesioned gut tissue of a patient with active Crohn's disease. For cell isolation from gut tissue, tissue was rinsed with PBS, treated with 0.15% DTT to remove mucous, then with 1 mM EDTA to remove epithelial cells and intra-epithelial lymphocytes. Remaining tissue was digested using Liberase-TL (Roche) plus 10 U/mL DNase I. Mononuclear cells were then filtered through 70 mM nylon filters and isolated via a 30%/ 70% Percol gradient. Mononuclear cells from blood or gut tissue were FACS-sorted into CD3+ CD4+ CD45RO+ MDR1+ or MDR1- memory T cells, using Rhodamine 123 (Rh123) efflux as a surrogate for MDR1 expression/ activity. Sorted cells were harvested directly ex vivo (without further in vitro culture or manipulation) prior to RNA extraction. MDR1- memory CD4+ T cells vs. MDR1+ memory CD4+ T cells from healthy donor peripheral blood or from active Crohn's disease lesioned tissue; MDR1- or MDR1+ memory CD4+ T cells from blood vs. inflamed gut tissue

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Expression profiling of MDR1+ and MDR1- human memory T cells from the blood and clinically-inflamed gut tissue

2013-12-17 | GSE49702 | GEO