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Mus musculus

ABSTRACT: ILC1 confer early host protection at initial sites of viral infection [ATAC-Seq]

PROVIDER: PRJNA407445 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6040940_1.fastq.gz	Fastqsanger.gz
	SRR6040940_2.fastq.gz	Fastqsanger.gz
	SRR6040941_1.fastq.gz	Fastqsanger.gz
	SRR6040941_2.fastq.gz	Fastqsanger.gz
	SRR6040942_1.fastq.gz	Fastqsanger.gz

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ILC1 confer early host protection at initial sites of viral infection

Project description:ILC1 confer early host protection at initial sites of viral infection

| PRJNA407437 | ENA

Mus musculus

Project description:ILC1 confer early host protection at initial sites of viral infection [RNA-Seq]

| PRJNA407446 | ENA

MCMV-experienced ILC1 acquire an m12-dependent memory response

Project description:Innate and adaptive immune cells can acquire “memory” of encounters with a diverse range of activating signals to tune their response to secondary stimuli. Group 1 innate lymphoid cells (ILC1) are recently discovered tissue-resident sentinels that are essential for early host protection from intracellular pathogens at initial sites of infection. However, whether ILC1 function as short-lived effectors or persist and refine their responsiveness following pathogen challenge is not well understood. Furthermore, whether pathogen-derived antigens directly modulate tissue-resident ILC responses remains unclear. Here, we found that liver-resident ILC1 expand locally and persist following the resolution of mouse cytomegalovirus (MCMV) infection. MCMVexperienced ILC1 acquired stable transcriptional, epigenetic, and phenotypic changes, with an enhanced protective effector response to secondary MCMV challenge. Protective memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, but not formed during bystander cytokine activation following heterologous infection. Thus, liver ILC1 acquire adaptive features in a MCMV-specific manner.

2019-05-02 | GSE128906 | GEO

ILC1 confer early host protection at initial sites of viral infection [RNA-Seq]

Project description:We show that tissue-resident ILC1 serve a non-redundant early role in host immunity through rapid production of interferon (IFN)-γ following mouse cytomegalovirus (MCMV) infection.

2017-11-01 | GSE103901 | GEO

ILC1 confer early host protection at initial sites of viral infection [ATAC-Seq]

2017-11-01 | GSE103900 | GEO

Lavigne2021 - Non-spatial model of viral infection dynamics and interferon response of well-mixed viral infection

Project description:This ordinary differential equation model is described in the following article: "Autocrine and paracrine interferon signalling as ‘ring vaccination’ and ‘contact tracing’ strategies to suppress virus infection in a host" G. Michael Lavigne, Hayley Russell, Barbara Sherry and Ruian Ke DOI: 10.1098/rspb.2020.3002 Comment: This model is based on the ordinary differential equations of the non-spatial model of well-mixed viral infection stated in the manuscript (Eq. 2.1 in the article). Abstract: The innate immune response, particularly the interferon response, represents a first line of defence against viral infections. The interferon molecules produced from infected cells act through autocrine and paracrine signalling to turn host cells into an antiviral state. Although the molecular mechanisms of IFN signalling have been well characterized, how the interferon response collectively contribute to the regulation of host cells to stop or suppress viral infection during early infection remain unclear. Here, we use mathematical models to delineate the roles of the autocrine and the paracrine signalling, and show that their impacts on viral spread are dependent on how infection proceeds. In particular, we found that when infection is well-mixed, the paracrine signalling is not as effective; by contrast, when infection spreads in a spatial manner, a likely scenario during initial infection in tissue, the paracrine signalling can impede the spread of infection by decreasing the number of susceptible cells close to the site of infection. Furthermore, we argue that the interferon response can be seen as a parallel to population-level epidemic prevention strategies such as ‘contact tracing’ or ‘ring vaccination’. Thus, our results here may have implications for the outbreak control at the population scale more broadly.

2024-09-02 | BIOMD0000001021 | BioModels

ATAC-Seq based chromatin accessibilty profile of MPPs from mice treated with MV130 or its excipient

Project description:MV130 is an inactivated polybacterial mucosal vaccine that confers protection to patients against recurrent respiratory infections, including those of viral etiology. We showed that MV130 induces long term heterologous protection against viral respiratory infections in mice. Moreover, intranasal administration of MV130 provided protection against systemic candidiasis in wild-type and Rag1-deficient mice lacking functional lymphocytes, indicative of innate immune-mediated protection. As trained immunity acts via modulation of hematopoietic stem and progenitor cells (Kaufmann et al., 2018; Mitroulis et al., 2018) we hypothesized that MV130 could confer systemic long-term protection through reprogramming of hematopoietic precursors. For that we measured the chromatin accessibility landscape in multipotent progenitors (MPPs) coming from mice treated with MV130 or its excipient using ATAC-seq.

2021-11-10 | GSE183486 | GEO

CITE-Seq analysis of total PBMC pre- and post-PfSPZ vaccination in the IMRAS trial

Project description:Immunization with radiation-attenuated sporozoites (RAS) can confer sterilizing protection against malaria, although the mechanisms behind this protection are incompletely understood. We performed a systems biology analysis of samples from the Immunization by Mosquito with Radiation Attenuated Sporozoites IMRAS) trial, which comprised P. falciparum RAS-immunized (PfRAS), malaria-naive participants whose protection from malaria infection was subsequently assessed by controlled human malaria infection (CHMI). Blood samples collected after initial PfRAS immunization were analyzed to compare immune responses between protected and non-protected volunteers leveraging integrative analysis of whole blood RNA-seq, high parameter flow cytometry, and single cell CITE-seq of PBMCs.

2022-02-01 | GSE191332 | GEO

ATAC-sequencing of Th1, Tfh, and memory-like splenic CD4+ T cells on day 14 post LCMV Cl13 infection

Project description:CD4+ T cell-derived interleukin 21 (IL-21) sustains CD8+ T cell responses during chronic viral infection, but the helper subset that confers this protection remains unclear. Here, we applied scRNA and ATAC-seq approaches to determine the heterogeneity of CD4+ T cells during LCMV clone 13 infection.

2022-02-25 | GSE193932 | GEO

Influenza-induced activation of recruited alveolar macrophages during the early inflammatory phase drives lung injury and lethality

Project description:we identify gene expression patterns associated with three distinct phases (Infiltrating, Early Inflammatory, Late Inflammatory) in the influenza A virus response of recruited alveolar macrophages. In the Early Inflammatory phase, recruited macrophages begin expressing pro-inflammatory genes, driving cytokine-mediated lung damage and contributing to the morbidity observed in influenza-infected wild-type mice. In mice lacking vimentin (Vim-/-), genes associated with the Early Inflammatory phase are suppressed, while the expression of the Infiltrating Phase genes is maintained, which is associated with protection from influenza-induced injury. Using a bone-marrow chimera mouse model, we validate that Vim-/- recruited alveolar macrophages are sufficient to confer protection from influenza-induced mortality. Our results define the temporal dynamics of gene expression in recruited alveolar macrophages, which shape the host response to infection with respiratory viruses.

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