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Mus musculus

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

PROVIDER: PRJNA407446 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6040950_1.fastq.gz	Fastqsanger.gz
	SRR6040950_2.fastq.gz	Fastqsanger.gz
	SRR6040960_1.fastq.gz	Fastqsanger.gz
	SRR6040960_2.fastq.gz	Fastqsanger.gz
	SRR6040951_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

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Mus musculus

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

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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.

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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.

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

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2024-08-01 | GSE182637 | GEO

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Inhalation of ACE2-expressing lung spheroid cell exosomes provides prophylactic protection against SARS-CoV-2

Project description:We demonstrated that lung spheroid cell derived exosomes (LSC-Exo) carry the parental cell’s ACE2 that are able to target lung, intercept SARS-CoV-2 entry, confer protection against SARS-CoV-2 infection. This LSC-Exo prophylaxis paradigm would not be limited by viral evolution, showing great potential for emerged SARS-CoV-2 variants, including those that are yet to emerge.

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