Mus musculus
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PROVIDER: PRJNA173236 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from WT and IL-2 secondary CD4 T cell effectors responding towards infuenza A virus infection
| PRJNA257695 | ENA
Project description:How secondary CD4 T cell effectors, derived from resting memory cells, differ from primary cells, derived from naïve precursors, and how such differences impact recall responses to pathogens is unknown. We used microarrays to detail the global programme of gene expression underlying differences between primary and secondary CD4 T cell effectors purified from the spleen, dLN, and lung on day 7 following A/PR8/34 influenza infection.
2012-08-27 | GSE40230 | GEO
Project description:Miao2010 - Innate and adaptive immune
responses to primary Influenza A Virus infection
This model is described in the article:
Quantifying the early immune
response and adaptive immune response kinetics in mice infected
with influenza A virus.
Miao H, Hollenbaugh JA, Zand MS,
Holden-Wiltse J, Mosmann TR, Perelson AS, Wu H, Topham DJ.
J. Virol. 2010 Jul; 84(13):
6687-6698
Abstract:
Seasonal and pandemic influenza A virus (IAV) continues to
be a public health threat. However, we lack a detailed and
quantitative understanding of the immune response kinetics to
IAV infection and which biological parameters most strongly
influence infection outcomes. To address these issues, we use
modeling approaches combined with experimental data to
quantitatively investigate the innate and adaptive immune
responses to primary IAV infection. Mathematical models were
developed to describe the dynamic interactions between target
(epithelial) cells, influenza virus, cytotoxic T lymphocytes
(CTLs), and virus-specific IgG and IgM. IAV and immune kinetic
parameters were estimated by fitting models to a large data set
obtained from primary H3N2 IAV infection of 340 mice. Prior to
a detectable virus-specific immune response (before day 5), the
estimated half-life of infected epithelial cells is
approximately 1.2 days, and the half-life of free infectious
IAV is approximately 4 h. During the adaptive immune response
(after day 5), the average half-life of infected epithelial
cells is approximately 0.5 days, and the average half-life of
free infectious virus is approximately 1.8 min. During the
adaptive phase, model fitting confirms that CD8(+) CTLs are
crucial for limiting infected cells, while virus-specific IgM
regulates free IAV levels. This may imply that CD4 T cells and
class-switched IgG antibodies are more relevant for generating
IAV-specific memory and preventing future infection via a more
rapid secondary immune response. Also, simulation studies were
performed to understand the relative contributions of
biological parameters to IAV clearance. This study provides a
basis to better understand and predict influenza virus
immunity.
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2021-10-05 | BIOMD0000000546 | BioModels
Project description:How secondary CD4 T cell effectors, derived from resting memory cells, differ from primary cells, derived from naïve precursors, and how such differences impact recall responses to pathogens is unknown. We used microarrays to detail the global programme of gene expression underlying differences between primary and secondary CD4 T cell effectors purified from the spleen, dLN, and lung on day 7 following A/PR8/34 influenza infection. Congenic naïve or in vivo influenza primed memory HNT TCR trangenic CD4 T cells were sort purifed from the spleens, dLNs, and lungs of infected mice on day 7 post infection for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain only CD4 T cell populations that had entered into the immune response by also sorting and collecting only those cells that had divided at least 5 times by CFSE analysis.
2012-08-27 | E-GEOD-40230 | biostudies-arrayexpress
Project description:How IL-2 produced by secondary CD4 T cell effectors, derived from resting memory cells, impacts memory CD4 T cell function and survival to memory following antigen re-encounter is unknown. We used microarrays to detail the global programme of gene expression underlying differences between WT and IL-2 deficient secondary CD4 T cell effectors purified from the lung on day 7 following A/PR8/34-OVAII influenza infection.
2015-05-14 | GSE60186 | GEO
Project description:How IL-2 produced by secondary CD4 T cell effectors, derived from resting memory cells, impacts memory CD4 T cell function and survival to memory following antigen re-encounter is unknown. We used microarrays to detail the global programme of gene expression underlying differences between WT and IL-2 deficient secondary CD4 T cell effectors purified from the lung on day 7 following A/PR8/34-OVAII influenza infection. Congenic primed memory DO11.10 TCR trangenic CD4 T cells were sort purifed from the lungs of infected mice on day 7 post infection for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain only CD4 T cell populations that had entered into the immune response by also sorting and collecting only those cells that had divided at least 5 times by CFSE analysis.
2015-05-14 | E-GEOD-60186 | biostudies-arrayexpress
Project description:To study the effects of secondary bacterial infection during 1918 pandemic H1N1 influenza virus infection, BALB/c mice were inoculated with the fully reconstructed 1918 influenza virus followed by inoculation with pneumococcus 72h later. To study the effects of secondary bacterial infection during 1918 pandemic H1N1 influenza virus infection, BALB/c mice were inoculated with the fully reconstructed 1918 influenza virus followed by inoculation with pneumococcus 72h later.
2015-09-20 | E-GEOD-70445 | biostudies-arrayexpress
Project description:Transcriptome analysis of CD4+ T cells responding to influenza infection.
2023-05-09 | GSE174103 | GEO
Project description:Chromatin accessibility analysis of CD4+ T cells responding to influenza infection.
2023-05-09 | GSE174101 | GEO
Project description:Thymic stromal lymphopoietin (TSLP) is a cytokine that acts directly on CD4+ T cells and dendritic cells to promote progression of asthma, atopic dermatitis, and allergic inflammation. However, a direct role for TSLP in CD8+ T-cell primary responses remains controversial and its role in memory CD8+ T-cell responses to secondary viral infection is unknown. Here, we investigate the role of TSLP in both primary and recall responses using two different viral systems. Interestingly, TSLP limited the primary CD8+ T cell response to influenza but did not affect T cell function nor significantly alter the number of memory CD8+ T cells generated after influenza infection. However, TSLP inhibited memory CD8+ T cell responses to secondary viral infection with influenza or acute systemic LCMV infection. These data reveal a previously unappreciated role for TSLP on recall CD8+ T cell responses in response to viral infection, findings with potential translational implications.
2021-01-05 | GSE156875 | GEO