Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126031 | ENA |
REPOSITORIES: ENA
Similar Datasets
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.
2012-10-17 | E-GEOD-39555 | biostudies-arrayexpress
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.
2012-10-17 | GSE39555 | GEO
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: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: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.
2020-04-28 | GSE149447 | GEO
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.
2013-04-03 | E-GEOD-45365 | biostudies-arrayexpress
Project description:Natural killer (NK) cells play a critical role in early host defense to infected and transformed cells. Here we show that mice deficient in Eri1, a conserved 3M-bM-^@M-^Y-to-5M-bM-^@M-^Y exoribonuclease that represses RNA interference, have a cell-intrinsic defect in NK cell development and maturation. Eri1M-bM-^@M-^S/M-bM-^@M-^S NK cells displayed delayed acquisition of Ly49 receptors in the bone marrow and a selective reduction in Ly49D and Ly49H activating receptors in the periphery. Eri1 was required for immune-mediated control of mouse cytomegalovirus (MCMV) infection. Ly49H+ NK cells deficient in Eri1 failed to expand efficiently during MCMV infection, and virus-specific responses were also diminished among Eri1M-bM-^@M-^S/M-bM-^@M-^S T cells. We identified miRNAs as the major endogenous small RNA target of Eri1 in mouse lymphocytes. Both NK and T cells deficient in Eri1 displayed a global, sequence-independent increase in miRNA abundance. Ectopic Eri1 expression rescued defective miRNA expression in mature Eri1M-bM-^@M-^S/M-bM-^@M-^S T cells. Thus, mouse Eri1 regulates miRNA homeostasis in lymphocytes and is required for normal NK cell development and anti-viral immunity. Small RNA profiling from wildtype and Eri1-deficient mouse CD4+ T cells
2012-07-11 | E-GEOD-31920 | biostudies-arrayexpress
Project description:This a model from the article:
Dynamics of killer T cell inflation in viral infections.
Wodarz D, Sierro S, Klenerman P. J R Soc Interface
2007 Jun 22;4(14):533-43 17251133
,
Abstract:
Upon acute viral infection, a typical cytotoxic T lymphocyte (CTL) response is
characterized by a phase of expansion and contraction after which it settles at
a relatively stable memory level. Recently, experimental data from mice infected
with murine cytomegalovirus (MCMV) showed different and unusual dynamics. After
acute infection had resolved, some antigen specific CTL started to expand over
time despite the fact that no replicative virus was detectable. This phenomenon
has been termed as "CTL memory inflation". In order to examine the dynamics of
this system further, we developed a mathematical model analysing the impact of
innate and adaptive immune responses. According to this model, a potentially
important contributor to CTL inflation is competition between the specific CTL
response and an innate natural killer (NK) cell response. Inflation occurs most
readily if the NK cell response is more efficient than the CTL at reducing virus
load during acute infection, but thereafter maintains a chronic virus load which
is sufficient to induce CTL proliferation. The model further suggests that
weaker NK cell mediated protection can correlate with more pronounced CTL
inflation dynamics over time. We present experimental data from mice infected
with MCMV which are consistent with the theoretical predictions. This model
provides valuable information and may help to explain the inflation of CMV
specific CD8+T cells seen in humans as they age.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D, Sierro S, Klenerman P. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2024-09-02 | BIOMD0000000688 | BioModels
Project description:This a model from the article:
Dynamics of killer T cell inflation in viral infections.
Wodarz D, Sierro S, Klenerman P. J R Soc Interface
2007 Jun 22;4(14):533-43 17251133
,
Abstract:
Upon acute viral infection, a typical cytotoxic T lymphocyte (CTL) response is
characterized by a phase of expansion and contraction after which it settles at
a relatively stable memory level. Recently, experimental data from mice infected
with murine cytomegalovirus (MCMV) showed different and unusual dynamics. After
acute infection had resolved, some antigen specific CTL started to expand over
time despite the fact that no replicative virus was detectable. This phenomenon
has been termed as "CTL memory inflation". In order to examine the dynamics of
this system further, we developed a mathematical model analysing the impact of
innate and adaptive immune responses. According to this model, a potentially
important contributor to CTL inflation is competition between the specific CTL
response and an innate natural killer (NK) cell response. Inflation occurs most
readily if the NK cell response is more efficient than the CTL at reducing virus
load during acute infection, but thereafter maintains a chronic virus load which
is sufficient to induce CTL proliferation. The model further suggests that
weaker NK cell mediated protection can correlate with more pronounced CTL
inflation dynamics over time. We present experimental data from mice infected
with MCMV which are consistent with the theoretical predictions. This model
provides valuable information and may help to explain the inflation of CMV
specific CD8+T cells seen in humans as they age.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D, Sierro S, Klenerman P. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2024-09-02 | BIOMD0000000687 | BioModels
Project description:This a model from the article:
Dynamics of killer T cell inflation in viral infections.
Wodarz D, Sierro S, Klenerman P. J R Soc Interface
2007 Jun 22;4(14):533-43 17251133
,
Abstract:
Upon acute viral infection, a typical cytotoxic T lymphocyte (CTL) response is
characterized by a phase of expansion and contraction after which it settles at
a relatively stable memory level. Recently, experimental data from mice infected
with murine cytomegalovirus (MCMV) showed different and unusual dynamics. After
acute infection had resolved, some antigen specific CTL started to expand over
time despite the fact that no replicative virus was detectable. This phenomenon
has been termed as "CTL memory inflation". In order to examine the dynamics of
this system further, we developed a mathematical model analysing the impact of
innate and adaptive immune responses. According to this model, a potentially
important contributor to CTL inflation is competition between the specific CTL
response and an innate natural killer (NK) cell response. Inflation occurs most
readily if the NK cell response is more efficient than the CTL at reducing virus
load during acute infection, but thereafter maintains a chronic virus load which
is sufficient to induce CTL proliferation. The model further suggests that
weaker NK cell mediated protection can correlate with more pronounced CTL
inflation dynamics over time. We present experimental data from mice infected
with MCMV which are consistent with the theoretical predictions. This model
provides valuable information and may help to explain the inflation of CMV
specific CD8+T cells seen in humans as they age.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D, Sierro S, Klenerman P. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2024-09-02 | BIOMD0000000686 | BioModels