Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257695 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data from primary and secondary CD4 T cell effectors responding towards influenza A virus infection
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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:Expression data from circulating and lung tissue resident memory CD4 T cell responding towards infuenza A virus infection
| PRJNA415081 | 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: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:The canonical pathway for IL-1? production requires TLR-mediated NF-?B-dependent Il1b gene induction, followed by caspase-containing inflammasome-mediated processing of pro-IL-1?. Here we show that IL-21 unexpectedly induces IL-1? production in conventional dendritic cells (cDCs) via a STAT3-dependent but NF-?B-independent pathway. IL-21 does not induce Il1b expression in CD4+ T cells, with differential histone marks present in these cells versus cDCs. IL-21-induced IL-1? processing in cDCs does not require caspase-1 or caspase-8 but depends on IL-21-mediated death and activation of serine protease(s). Moreover, STAT3-dependent IL-1? expression in cDCs at least partially explains the IL-21-mediated pathologic response occurring during infection with Pneumonia Virus of Mice. These results demonstrate lineage-restricted IL-21-induced IL-1? via a non-canonical pathway and provide evidence for its importance in vivo. Genome-wide transcription factors mapping and binding of STAT3, H3K4me3, H3K27me, H3K4me1, H3K27ac in mouse CD4+ T cells and dendritic cells in WT and Stat3-/- mice. RNA-Seq is performed in mouse CD4+ T cells and dendritic cells in WT mice, with or without indicated cytokines.
2015-07-07 | E-GEOD-61677 | biostudies-arrayexpress
Project description:Transcriptome analysis of CD4+ PD1+ T cells during LCMV CL13 infection Gene expression in WT and ERt2-cre;TGFbRII flox virus specific CD4 T cells
2016-06-30 | GSE83921 | GEO
Project description:CD4⁺ T cells are believed to be essential for effective CD8⁺ T cell responses against hepatotropic viruses like hepatitis B virus (HBV). However, the specific locations and the cellular and molecular mechanisms through which CD4⁺ T cells help CD8⁺ T cells remain unclear. In this study, we generated HBV-specific CD4⁺ TCR transgenic mice to demonstrate that effector CD4⁺ T cells can prevent or reverse the dysfunction of CD8⁺ T cells caused by hepatocellular priming. This, in turn, enhances CD8⁺ T cell effector function and suppresses viral replication. Notably, CD4⁺ T cell help to CD8+ T cells occurs directly in the liver, independent of secondary lymphoid organs, and requires local antigen recognition but not epitope linkage. While dendritic cells were found to be dispensable, Kupffer cells (KCs) emerged as the critical cellular platform for this effect. Mechanistically, CD4⁺ T cells engage KCs via CD40-CD40L interactions, leading to the production of IL-12 and IL-27. IL-12 promotes further CD4⁺ T cell expansion, whereas IL-27 serves as the key cytokine that restores CD8⁺ T cell functionality. Furthermore, we show that exogenous IL-27 administration can reverse HBV-specific CD8⁺ T cell dysfunction in mice and in chronically infected patients. These findings reveal a novel mechanism of CD4⁺ T cell help to CD8⁺ T cells that occurs outside secondary lymphoid organs, specifically in the liver, and involves antigen-presenting cells other than conventional dendritic cells, offering new insights for immunotherapeutic strategies against chronic HBV infection.
2025-05-03 | GSE283038 | GEO
Project description:Understanding the response of memory CD8 T cells to persistent antigen re-stimulation and the role of CD4 T cell help is critical to the design of successful vaccines for chronic diseases. However, studies comparing the protective abilities and qualities of memory and naïve cells have been mostly performed in acute infections, and little is known about their roles during chronic infections. Herein, we show that memory cells dominate over naïve cells and are protective when present in large enough numbers to quickly reduce infection. In contrast, when infection is not rapidly reduced, memory cells are quickly lost, unlike naïve cells. This loss of memory cells is due to (i) an early block in cell proliferation, (ii) selective regulation by the inhibitory receptor 2B4, and (iii) increased reliance on CD4 T cell help. These findings have important implications towards the design of T cell vaccines against chronic infections and tumors. 16 samples are analyzed: 3 replicates of secondary effector CD8 P14 T cells at day 8 post-acute lymphocytic choriomeningitis virus (LCMV) infection; 4 replicates of secondary effector CD8 P14 T cells at day 8 post-chronic LCMV infection; 4 replicates of primary effector CD8 P14 T cells at day 8 post-acute LCMV infection; and 5 replicates of primary effector CD8 P14 T cells at day 8 post-chronic LCMV infection.
2011-08-22 | E-GEOD-30962 | biostudies-arrayexpress