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ILC1 confer early host protection at initial sites of viral infection

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

PROVIDER: PRJNA407437 | ENA |

REPOSITORIES: ENA

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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

ILC1 Confer Early Host Protection at Initial Sites of Viral Infection.

Project description: Not available

| S-EPMC5687850 | biostudies-literature

ILC1 confer early host protection at initial sites of viral infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-11-01 | GSE103904 | GEO

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

Mus musculus

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

| PRJNA407445 | ENA

Mus musculus

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

| PRJNA407446 | ENA

Gene expression analysis of CD4+ and CD4- ILC1 subsets by RNAseq

Project description:Innate lymphoid cell (ILC) subsets that mirror helper T cells in their effector cytokine profiles have recently emerged as central players in both homeostatic and inflammatory conditions. Like their Th1, Th2 and Th17/Th22 helper T cell counterparts, ILC subsets are categorized based on their expression of specific transcription factors and effector cytokines: group 1 ILC (ILC1) express T-bet and IFN-Î³; group 2 ILC (ILC2) express GATA-3 and type 2 effector cytokines such as IL-13 and IL-5; and group 3 ILC (ILC3) express RORgt and the cytokines IL-22 and/or IL-17. Under this nomenclature, natural killer (NK) cells and lymphoid tissue inducers (LTi) are considered ILC1 and ILC3, respectively. ILC1 contain both CD4+ and CD4- populations, but whether this phenotypic characteristic reflects functional differences between these two populations is unknown. These studies examine the gene expression profiles of CD4+ vs CD4- ILC1 in a cohort of healthy control subjects. ILC subsets were isolated from the peripheral blood of healthy control subjects. cDNA was isolated and amplified from sorted populations, and gene expression was analyzed by RNAseq

2015-12-31 | E-GEOD-69596 | biostudies-arrayexpress

Monocyte-derived alveolar macrophages induced by influenza infection confer long-term antibacterial protection

Project description:Monocyte-derived alveolar macrophages induced by influenza infection confer long-term antibacterial protection

| PRJNA493387 | ENA

Divergent roles for STAT4 in shaping effector differentiation of ILC1 and NK cells during gut inflammation II

Project description:Natural killer (NK) cells and type 1 innate lymphoid cells (ILC1) require the transcription factor STAT4 to elicit rapid effector responses and protect against pathogens. Herein, by combining genetic and transcriptomic approaches, we revealed that STAT4 played an unexpected divergent role in regulating effector differentiation of murine ILC1 and NK cells, during intestinal inflammation. Stat4 deletion in Ncr1-expressing cells led to an increased generation of cytotoxic ILC1 in the inflamed large intestine. By contrast, Stat4-deficient NK cells showed impaired terminal differentiation, characterized by lower levels of IRF-8 and KLRG1. STAT4 expression in NCR+ innate lymphocytes restrained gut inflammation and controlled both systemic IFN-g levels and the number of type 2 adaptive T cells in the large intestine. Collectively our data shed light on shared and distinctive mechanisms of transcriptional regulation driven by STAT4 in NK cells and ILC1 required for protection during intestinal inflammation.

2023-09-28 | GSE210977 | GEO

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