Avidity Selection of Natural Killer Response to MCMV
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ABSTRACT:
PROVIDER: PRJNA531485 | ENA |
REPOSITORIES: ENA
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Project description:Natural killer (NK) cells are innate lymphocytes that possess features of adaptive immunity, such as the ability to recognize specific antigen, among others. In MCMV infection, the engagement of a subset of NK cells expressing an activating receptor Ly49H with MCMV-derived glycoprotein m157 results in a clonal-like expansion and the generation of a small pool of long-lived memory cells with higher Ly49H expression than the naive Ly49H-expressing NK cell pool. In this study, we interrogate the transcriptional differences between NK cells that express high verus low levels of Ly49H early after infection.
2019-04-09 | GSE129490 | GEO
Project description:Regulation of natural killer cells during MCMV infection
| PRJNA415717 | ENA
Project description:Investigation of global gene expression levels between B cells, Natural killer cells and Natural killer B cells Gene expression profiling using sorted B cells, Natural killer cells and Natural killer B cells from WT mouse spleen. Total RNA extracted from WT cells were quantified by the NanoDrop ND-1000 and RNA integrity was assessed by standard denaturing agarose gel electrophoresis. The sample preparation and microarray hybridization were performed based on the NimbleGenâs standard protocols.
2016-05-17 | E-GEOD-80063 | biostudies-arrayexpress
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
Project description:Dendritic cells (DCs) are a complex group of cells which play a critical role in vertebrate immunity. They are subdivided into conventional DC (cDC) subsets (CD11b and CD8alpha in mouse) and plasmacytoid DCs (pDCs). Natural killer cells are innate lymphocytes involved in the recognition and killing of abnormal self cells, including virally infected cells or tumor cells. DCs and NK cells are activated very early upon viral infections and regulate one another. However, the global responses of DC and NK cells early after viral infection in vivo and their molecular regulation are not entirely characterized. The goal of this experiment was to use global gene expression profiling to assess the global genetic reprogramming of DC and NK cells during a viral infection in vivo, as compared to B lymphocytes, and to investigate the underlying molecular mechanisms This study includes data from cell sort purified DCs, NK cells and B cells isolated from the spleen of MCMV-infected mice. 2 independent replicates were made for each cell type except B cells. The control dataset for cells isolated from uninfected control animals has been previously published and is available in the GEO database as GSE9810. The complete dataset representing: (1) the infected Samples and (2) the uninfected control Samples from Series GSE9810 (re-processed using RMA), is linked below as a supplementary file. Comparison of the gene expression programs of wild-type spleen leukocyte subsets, including plasmacytoid DCs, CD8alpha conventional DCs, CD11b conventional DCs and NK cells, isolated from MCMV-infected versus control animals.
2012-10-17 | E-GEOD-21491 | biostudies-arrayexpress
Project description:Investigation of global gene expression levels between B cells, Natural killer cells and Natural killer B cells
2016-05-17 | GSE80063 | GEO
Project description:Comparing global gene expression of neonatal and adult natural killer cells to determine if differences in gene expression suggest that different developmental pathways during hematopoiesis are followed in the fetal and adult mouse to produce mature natural killer cells.
2005-10-01 | E-MEXP-354 | biostudies-arrayexpress
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).
2015-04-24 | GSE62729 | GEO
Project description: Not available
| S-EPMC6614060 | biostudies-literature
Project description:Natural killer (NK) cells are innate lymphocytes that have been recently appreciated to display features of adaptive immunity in response to viral infection. Biallelic mutations in the IRF8 gene have been reported to cause familial NK cell deficiency and susceptibility to severe viral infection in humans; however, the precise role of this transcription factor in regulating NK cell function remained unknown. Here, we show that IRF8 is required in a cell-intrinsic manner for NK cell-mediated protection against mouse cytomegalovirus (MCMV) infection. During exposure to MCMV, IRF8 is robustly upregulated in NK cells by IL-12 and STAT4, which promotes epigenetic remodeling of the Irf8 locus. Moreover, IRF8 facilitates the proliferative burst of virus-specific NK cells by promoting expression of a suite of DNA replication and cell cycle genes, and directly regulating Zbtb32, a master regulator of NK cell proliferation during viral challenge. These results identify a novel function and cell-type specific regulation for IRF8 in host antiviral immunity, and provide a mechanistic understanding of virus susceptibility in patients with IRF8 mutations.
2018-05-16 | GSE112948 | GEO