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Shared and distinct metabolic demands for innate and adaptive cytotoxic lymphocytes during viral infection

ABSTRACT: Natural Killer (NK) cells and CD8+ T cells share many characteristics at steady state and during viral infection. In this study, we interrogate the metabolic pathways that fuel NK cell effector function in response to mouse cytomegalovirus (MCMV) infection. This dataset contains transcriptional profiling of wild-type and LDHA-deficient Ly49Hpositive NK cells at steady state and early after infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE149447 | GEO | 2020/04/28

REPOSITORIES: GEO

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Natural killer cell sensing of infected cells compensates deficient Toll-like receptor but not IFN-I activity for mouse resistance to cytomegalovirus

Project description:Plasmacytoid dendritic cells (pDC) are the major source of type I IFN (IFN-I) in vivo during Murine Cytomegalovirus (MCMV) infection. This response requires pDC-intrinsic MyD88-dependent signaling by Toll Like Receptors 7/9. Provided that they express appropriate recognition receptors such as Ly49H, Natural Killer (NK) cells can directly sense and kill MCMV-infected cells. While MyD88- and Ly49H-dependent responses can contribute to MCMV control, the objective is to understand the relative importance of these 3 mechanisms. In order to decipher the relative impact of MyD88- and Ly49H-dependent mechanisms during MCMV infection, we performed a genome-wide expression analysis on total spleen of Ly49H-/-MyD88+/+, Ly49H-/-MyD88-/-, Ly49H+/+MyD88+/+ and Ly49H+/+MyD88-/- BALB/c mice at different time points after MCMV infection (d0, d1,5, d2, d3 and d6). This study includes data from the spleen BALB/c mice, under steady-state or MCMV condition at different time points. 2 to 5 mice for each mouse strain for each time point were used, and were hybridized on 5 separate batches of gene chips.

2015-04-24 | E-GEOD-62729 | biostudies-arrayexpress

Genome-wide expression study of the responses of murine NK cells and dendritic cell subsets to MCMV infection

Project description:Murine Cytomegalovirus (MCMV) infection leads to the activation of various immune cells, including dendritic cells (DCs) and Natural Killer (NK) cells. This activation is partly driven by innate cytokines including IFN-I, which are induced early after infection. The objective was to address the role of different innate cytokines in shaping DC subsets and NK cell responses, in particular the role of cell intrinsic responses to IFN-I. In order to decipher the specific impact of cell-intrinsic IFN-I on cell subsets, we performed a genome-wide expression analysis on CD45.1 WT and CD45.2 IFNAR-/- splenic conventional DC (cDC) subsets and NK cells isolated from C57BL/6 [CD45.1 WT / CD45.2 IFNAR-KO] mixed bone marow chimera mice. This study includes data from cDC subsets (CD8a and CD11b) and NK cells purified by flow cytometry sorting from the spleen of bone marrow chimera (BMC) mice, under steady-state or MCMV condition. Two independent replicates were made for each cell type, from two independent pools of spleens from uninfected or d1.5 MCMV-infected BMC 5-8 mice, and were hybridized on 3 separate batches of gene chips.

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scRNA-Seq of negatively enriched NK cells 4 days post MCMV infection

Project description:Ly49G2+ NK cells mediate essential control of murine cytomegalovirus (MCMV) infection in mice which express the H-2Dk class I molecule. As a cognate ligand for specific Ly49G2 inhibitory receptor allotypes, H-2Dk also licenses Ly49G2+ NK cells in naïve and MCMV-infected mice. These findings suggest Ly49G2 may promote antiviral NK cell activities during MCMV infection. Indeed, in mice lacking the Ly49G2 receptor, MCMV resistance is fully abrogated. Additionally, NK cells expressing Ly49R, an NK cell associated activation receptor that also recognizes H-2Dk, have their function augmented by Ly49G2 and are required for MCMV resistance.

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Genome-wide expression study of the early/innate responses of murine B and T cells to MCMV infection

Project description:Murine Cytomegalovirus (MCMV) infection leads to early activation of various immune cells, including B and T lymphocytes, before the actual initiation of antigen-specific adaptive immunity. This activation is partly driven by innate cytokines, including type I interferon (IFN), which are induced early after infection. The objective of this study was to address the role of type I IFN in shaping early/innate B and T cell responses to a primary acute viral infection. In order to decipher the specific impact of IFN-I on cell subsets, we performed a genome-wide expression analysis on WT splenic B and CD8 T lymphocytes isolated from C57BL/6 [CD45.1 WT / CD45.2 IFNAR-KO] mixed bone marrow chimera mice. This study complements series GSE39555, which focused on early responses of NK cells and of the two subsets of conventional dendritic cells. This study includes data from B and CD8 T lymphocytes purified by flow cytometry sorting from the spleen of bone marrow chimera (BMC) mice, under steady-state or MCMV conditions. Two independent replicates were made for each cell type, from two independent pools of spleens from uninfected or d1.5 MCMV-infected BMC 5-8 mice, and were hybridized on 3 separate batches of GeneChips.

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Project description:Upon viral infection, NK cells expressing certain germline-encoded receptors are selected, expanded and maintained in an adaptive-like manner. Currently, these are thought to differentiate along a common pathway. However, by fate mapping of single NK cells upon murine cytomegalovirus (MCMV) infection, we identified two distinct NK cell lineages that contributed to adaptive-like responses. One was equivalent to conventional NK (cNK) cells while the other was transcriptionally similar to type 1 innate lymphoid cells (ILC1s). ILC1-like NK cells showed splenic-residency and strong cytokine production but also recognized and killed MCMV-infected cells, guided by activating receptor Ly49H. Moreover, they induced clustering of conventional type 1 dendritic cells and facilitated antigen-specific T cell priming early during MCMV infection, which depended on Ly49H and the NK cell-intrinsic expression of transcription factor Batf3. Thereby, ILC1-like NK cells bridge innate and adaptive viral recognition and unite critical features of cNK cells and ILC1s.

2021-08-25 | GSE180976 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [scRNAseq_spleen_Ly49H+_steady-state]

2021-08-25 | GSE180975 | GEO

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2021-08-25 | GSE180974 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [bulk_RNAseq_steady_state]

2021-08-25 | GSE180973 | GEO

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Proliferation conditions promote intrinsic changes in NK Cells for an IL-10 response

Project description:Constitutively found at high frequencies, the role for NK cell proliferation remains unclear. Here, a shift in NK cell function from predominantly producing interferon-? (IFN-?), a cytokine with proinflammatory and antimicrobial functions, to producing the immunoregulatory cytokine IL-10, is defined during extended murine cytomegalovirus infection. The NK cells driven to express IL-10 in vivo acquired responsiveness to IL-12 and IL-21 for IL-10 production, but neither cytokine was required for the endogenous response. In vitro studies with IL-2 to support proliferation and in vivo adoptive transfers into murine cytomegalovirus-infected mice demonstrated that NK cell proliferation and further division enhanced the change. During infection, the responding NK cells acquired histone modifications indicative of an open IL-10 gene, and an IL-10 response was proliferation dependent ex vivo if the NK cells had not yet expanded in vivo but independent if they had. Thus, a novel role for proliferation in supporting changing innate cell function is discovered. The chromatin status of ex vivo isolated NK cells during MCMV infection was investigated by ChIP-seq on histone epigenetic marks (H3K4m3, H3K27m3, H3K36m3) on day 0, day 1.5 and day 3.5 post infection.

2014-08-05 | E-GEOD-55834 | biostudies-arrayexpress

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