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Gene transcription and chromatin accessibility of conventional NK cells and ILC1s in spleens of uninfected and Toxoplasma gondii-infected Mice

ABSTRACT: Gene transcription and chromatin accessibility of conventional NK cells and ILC1s in spleens of uninfected and Toxoplasma gondii-infected Mice

PROVIDER: PRJNA511586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8366740.fastq.gz	Fastqsanger.gz
	SRR8366750_1.fastq.gz	Fastqsanger.gz
	SRR8366750_2.fastq.gz	Fastqsanger.gz
	SRR8366741.fastq.gz	Fastqsanger.gz
	SRR8366751_1.fastq.gz	Fastqsanger.gz

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Gene transcription and chromatin accessibility of conventional NK cells and ILC1s in spleens of uninfected and Toxoplasma gondii-infected Mice

Project description:RNA sequencing and ATAC-seq of conventional NK cells and ILC1s in uninfected mice and mice that were infected 5 wk previously with the Type II Prugniaud strain of T. gondii

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Toxoplasma gondii Infection Promotes NK Cell Conversion into ILC1s and Heterogeneous ILC1 Populations

Project description:Innate lymphoid cells (ILCs) comprise several subsets that were originally classified based on their cytokine production profiles. Natural killer (NK) cells and type 1 ILCs (ILC1s) were initially classified together, but recent data supported their separation into different lineages. Here we describe how infection with the parasite Toxoplasma gondii induces changes to NK1.1+ NKp46+ cells that persist independent of ongoing infection. Notably, there is an expansion of Eomes– CD49a+ cells that superficially resemble ILC1s, but express unique genes, circulate throughout the vasculature, and possess distinct epigenetic marks. Single-cell RNA sequencing confirms T. gondii-induced Eomes– CD49a+ cells are distinct from both conventional NK cells and ILC1s. Furthermore, there is heterogeneity within this population, as both conventional NK cells and ILC1s contribute to their formation. Indeed, downregulation of Eomes within conventional NK cells accounts for most T. gondii-induced Eomes– CD49a+ cells, indicating that NK cells can give rise to cells resembling ILC1s during infection.

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Project description:The objectives of the present study were to analyze the changes on miRNA expression profile in swine spleen using next-generation sequencing (NGS) technology and bioinformatic analysis at 10, 25 and 50 days post inoculation (DPI) with Chinese I genotype strain of T. gondii. Compared to control group, 34, 6 and 86 differentially expressed miRNAs (DEMs) were respectively found in spleens of infected pigs at 10, 25 and 50 DPI. The results not only showed that the miRNA expression of the host can be changed by the invasion of T. gondii, but also revealed the differences on the regulation of the key biological processes or pathways involved in host responses between the acute and chronic T. gondii infection.

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Role of Bcl3 in Dendritic cell function in the context of Toxoplasma gondii infection

Project description:This experiment contains two mice genotypes – WT and Bcl3 flx/flx Zbtb46 cre knockouts (both C57BL/6 background). These mice were either infected with 15 cysts of Toxoplasma gondii (ME49 strain) or kept uninfected. Spleens were harvested from mice 7 days post infection and splenocytes were isolated. With four experimental groups (KO/WT and infected/uninfected) and two biological replicate mice per group, we have a total of 8 biological samples comprising of single cell suspensions of splenocytes enriched for CD11c. Single cell RNA-seq libraries were prepared from CD11c-enriched single cells using the Chromium Single Cell 3’ Reagent Kits v3 (10X Genomics; Pleasanton, CA, USA). Eight sample libraries were multiplexed and sequenced 100bp paired end in four different runs of Illumina NextSeq2000, followed by demultiplexing that resulted in multiple raw FASTQ files corresponding to paired reads (R1 and R2), index barcodes (I1) and four sequencing runs (Seq1 - Seq4). The main goal of this project was to define Bcl3-associated transcriptional responses in dendritic cells during T. gondii infection.

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Toxoplasma gondii Infection Promotes NK Cell Conversion into ILC1s and Heterogeneous ILC1 Populations

Project description:Toxoplasma gondii Infection Promotes NK Cell Conversion into ILC1s and Heterogeneous ILC1 Populations

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