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Identification of pathogenic TRAIL-expressing innate immune cells during HIV-1 infection in humanized mice by scRNA-seq

ABSTRACT: Identification of pathogenic TRAIL-expressing innate immune cells during HIV-1 infection in humanized mice by scRNA-seq

PROVIDER: PRJNA625738 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11557449.fastq.gz	Fastqsanger.gz
	SRR11557450.fastq.gz	Fastqsanger.gz
	SRR11557451.fastq.gz	Fastqsanger.gz
	SRR11557452.fastq.gz	Fastqsanger.gz
	SRR11557453.fastq.gz	Fastqsanger.gz

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Identification of pathogenic TRAIL-expressing innate immune cells during HIV-1 infection in humanized mice by scRNA-seq

Project description:We employed the single-cell RNA sequencing (scRNA-seq) technology to study HIV-induced transcriptomic change in innate immune cells in lymphoid organs. We performed scRNA-seq on hCD45+hCD3-hCD19- human leukocytes isolated from spleens of humanized NOD/Rag2-/- /γc-/- (NRG) mice transplanted with human CD34+ hematopoietic stem-progenitor cells (NRG-hu HSC mice). We identified major populations of innate immune cells including plasmacytoid dendritic cells (pDC), myeloid dendritic cells (mDC), macrophage, nature killer (NK) cells and innate lymphoid cells (ILC). HIV-1 infection significantly upregulated genes involved in type-I interferon inflammatory pathways in each of the innate immune subsets. Interestingly, we found that the TNF-related apoptosis-inducing ligand (TRAIL) was upregulated in the innate immune populations including pDC, mDC, macrophage, NK and ILC. In summary, we characterized HIV-induced transcriptomic changes of innate immune cells in the spleen at single-cell levels, identified the TRAIL+ innate immune cells and defined an important role of TRAIL signaling pathway in HIV-1 induced CD4+ T cell depletion in vivo.

2020-06-04 | GSE148796 | GEO

Identification of pathogenic TRAIL-expressing innate immune cells during HIV-1 infection in humanized mice by scRNA-Seq.

Project description:Depletion of CD4+ T cells during HIV-1 infection is mostly mediated by inflammatory cells via indirect but not clearly defined mechanisms. In this report, we used single-cell RNA-Seq (scRNA-Seq) technology to study HIV-induced transcriptomic change in innate immune cells in lymphoid organs. We performed scRNA-Seq on hCD45+hCD3-hCD19- human leukocytes isolated from spleens of humanized NOD/Rag2-/-γc-/- (NRG) mice transplanted with human CD34+ hematopoietic stem progenitor cells (NRG-hu HSC mice). We identified major populations of innate immune cells, including plasmacytoid dendritic cells (pDCs), myeloid dendritic cells (mDCs), macrophages, NK cells, and innate lymphoid cells (ILCs). HIV-1 infection significantly upregulated genes involved in type I IFN inflammatory pathways in each of the innate immune subsets. Interestingly, we found that TRAIL was upregulated in the innate immune populations, including pDCs, mDCs, macrophages, NK cells, and ILCs. We further demonstrated that blockade of the TRAIL signaling pathway in NRG-hu HSC mice prevented HIV-1-induced CD4+ T cell depletion in vivo. In summary, we characterized HIV-induced transcriptomic changes of innate immune cells in the spleen at single-cell levels, identified the TRAIL+ innate immune cells, and defined an important role of the TRAIL signaling pathway in HIV-1-induced CD4+ T cell depletion in vivo.

| S-EPMC7308046 | biostudies-literature

TRAIL expressing monocyte/macrophages reduce inflammation and attenuate atherosclerosis

Project description:Circulating TRAIL is reduced in cardiovascular disease patients and TRAIL deletion in mice exacerbates disease. The source of TRAIL and protective mechanism(s) are unclear. Monocyte TRAIL mRNA was reduced from coronary artery disease patients, strikingly associating with reduced plasma TRAIL. A strong inverse correlation between plasma TRAIL and IL-18 was observed, with IL-18 repressing monocyte TRAIL mRNA. In mice, two sources were investigated using bone-marrow (BM) transplants; TRAIL expressed only in BM (BM-TRAIL) or everywhere except BM (parenchymal-TRAIL), vs. whole-body TRAIL ablation (null-TRAIL). BM-TRAIL attenuated macrophage content and atherosclerosis. BM-derived macrophages with TRAIL deletion were more inflammatory, with impaired migration and reduced expression of cholesterol efflux, efferocytosis and nitric oxide-controlling genes. TRAIL expression also reduced islet macrophage content, but only parenchymal-TRAIL islets had improved function. Recombinant TRAIL administration stimulated insulin expression and islet mass. We propose TRAIL maintains monocyte/macrophage homeostasis and limits the progression of atherosclerosis and islet dysfunction.

2019-12-03 | GSE107645 | GEO

microRNA expression of TRAIL-sensitive and TRAIL-resistant Bel-7402 cells

Project description:To further analyze the change of microRNA (miRNA) between TRAIL-sensitive and TRAIL-resistant Bel-7402 cells Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)

2015-10-20 | GSE74130 | GEO

Transcription profiling of bronchus from macaques infected with either the 1918 influenza virus or a humanized contemporary H1N1 influenza virus

Project description:The 1918 influenza pandemic was unusually severe, resulting in about 50 million deaths worldwide. A reconstructed version of the 1918 (H1N1) virus has been shown to also highly pathogenic in mice; however, the potential virulence and pathogenicity of the 1918 virus in nonhuman primates in unknown. In these studies, we demonstrate that the 1918 virus caused a highly pathogenic respiratory infection in a cynomolgus macaque model that culminated in acute respiratory distress and a fatal outcome. To characterize the global gene expression host response, oligonulceotide microarray analysis was performed on RNA isolated from the bronchus of macaques infected with either the 1918 virus or a humanized contemporary H1N1 influenza virus (A/Kawasaki/173/01). These experiments showed that infected animals mounted an immune response, characterized by dysregulation of the antiviral response, that was insufficient for protection, suggesting that atypical host innate immune responses may contribute to lethality.

2007-01-18 | E-TABM-181 | biostudies-arrayexpress

Comparison of Trail+/+ versus Trail-/- splenic NK cells from naïve and LCMV-infected mice

Project description:Investigation of the change of the Trail-dependent NK cell transcriptome during short-term (24h) infection with lymphocytic choriomeningitis virus (LCMV). RNA sequencing-based transcriptomics analysis was performed in spleen-isolated (NK1.1+CD3-) NK cells from 3 naïve Trail+/+ mice, 3 naive Trail-/- mice, 4 LCMV-infected Trail+/+ mice, and 4 LCMV-infected Trail-/- mice.

2019-08-27 | E-MTAB-7562 | biostudies-arrayexpress

Transcription profiling of human TRAIL-resistant metastatic vs primary TRAIL-sensitive melanoma cells

Project description:T1 and G1 are the two melanoma cell lines, established from primary tumor (T1) and lymph node metastases (G1) of a 77 years old male patient. While G1 cells were resistant to TRAIL (TNF-related apoptosis-inducing ligand) mediated cell death, T1 cells exhibited a high dose- and time-dependent sensitivity to TRAIL. Cells were treated with or without of two doses (0.2 and 1ug/ml) of TRAIL for 24 h. Gene expression of each sample vs pool was measured. TRAIL-resistant metastatic G1 vs primary TRAIL-sensitive T1 was compared.

2006-01-01 | E-MEXP-247 | biostudies-arrayexpress

Proteomic analysis of TRAIL-induced endogenous RIPK3-dependent necrosome complex

Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a well-known inducer of apoptosis via formation of the primary death-inducing signaling complex (TRAIL-DISC) at the level of membrane death receptors (DR4 and DR5) which recruit successively FADD and caspase-8. TRAIL can also induce necroptosis when caspases are inhibited. Necroptosis is a regulated cell death dependent on the formation of a cytosolic necrosome complex which includes RIPK1, RIPK3 and MLKL proteins. Elucidating the molecular mechanisms involved in TRAIL-induced necroptosis might provide new insights into the TRAIL death signaling pathway. Here, we report the analysis by mass spectrometry of endogenous RIPK3-dependent necrosome complex constituents upon necroptosis induced by TRAIL/z-VAD/Birinapant (TzB) in HT29 cells. Besides characterization of RIPK1, RIPK3, MLKL, FADD, caspase-8, we find TRIM21 as a new constituent of the necrosome complex. Moreover RIPK1, RIPK3, MLKL, P-MLKL, FADD, caspase-8 and TRIM21 are also found associated to the native TRAIL-DISC upon TzB stimulation showing initiation of the necrotic pathway at the level of TRAIL death receptors in HT29 cells. Finally, TRIM21 may positively modulate necroptosis induction by downregulating NF-kB activation.

2021-03-18 | PXD003383 | Pride

TRAIL-induced cancer secretome

Project description:To comprehensively determine which factors are secreted by cancer cells upon TRAIL stimulation, we conducted an unbiased mass spectrometric analysis of TRAIL’s secretome in resistant A549 cells.

2017-12-19 | PXD005664 | Pride

Gene expression profile of TRAIL-sensitive and -resistant H460 cells

Project description:We generated H460 cells with acquired TRAIL resistance by exposing the parental sentisitve cells to subtoxic concentrations of TRAIL for 6 months. Then we compared the gene expression profile of the sensitive versus the resistant cells. We generated acquired TRAIL-resistant H460 cells from the sentisitve cells by treating subtoxic range of TRAIL for 6 month. And we tried to compare the expressional profile of the genes between two cell types to isolate genes regulating acquired TRAIL-resistance

2014-09-01 | GSE55859 | GEO

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