ChIP Seq of influenza specific primary, memory and secondary CD4+ T cells [In Vivo]
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PROVIDER: PRJNA558171 | ENA |
REPOSITORIES: ENA
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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:ChIP Seq of influenza specific primary, memory and secondary CD4+ T cells
| PRJNA558080 | 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:ChIP Seq of influenza specific primary, memory and secondary CD4+ T cells [InVitro]
| PRJNA558167 | ENA
Project description:Immune responses to infection involve a careful balance: too weak a response allows pathogen replication; too strong risks immunopathology. The immunoregulatory cytokine IL-10 is a key factor in this balance, but the impact of IL-10 is context-dependent and current understanding of the factors that regulate IL-10 is incomplete. In this study, we demonstrated that the infection induced cytokine IL-27 promotes IL-10 expression in CD4+ T cells by directing epigenetic changes in H3K4me3, H3K27me3, H3K4me1 and H3K27Ac modifications at the Il10 locus. We showed that primary activation of antigen-specific CD4+ T cells, in the context of murine influenza infection, led to the long-term remodelling of the epigenetic landscape at both the Il10 promoter and a distinct active enhancer element ~ 25 kb upstream of the TSS. Intact IL-27 signalling was an essential requirement for these persistent epigenetic changes in memory CD4+ Tcells. We identified CREB1 as a transcription factor binding the Il10 active enhancer, and we showed that the ability of IL-27 to promote IL-10 expression was dependent on the histone acetyl transferase activity of the CREB1 complex member, p300. Together our data provide mechanistic insight into the action of IL-27 in regulating an immune response. We suggest that infection-induced cytokine signals direct epigenetic changes that moderate cytokine output in response to T cell receptor stimulation, regulating immune activity at sites of infection.
2022-12-31 | GSE135249 | GEO
Project description:Immune responses to infection involve a careful balance: too weak a response allows pathogen replication; too strong risks immunopathology. The immunoregulatory cytokine IL-10 is a key factor in this balance, but the impact of IL-10 is context-dependent and current understanding of the factors that regulate IL-10 is incomplete. In this study, we demonstrated that the infection induced cytokine IL-27 promotes IL-10 expression in CD4+ T cells by directing epigenetic changes in H3K4me3, H3K27me3, H3K4me1 and H3K27Ac modifications at the Il10 locus. We showed that primary activation of antigen-specific CD4+ T cells, in the context of murine influenza infection, led to the long-term remodelling of the epigenetic landscape at both the Il10 promoter and a distinct active enhancer element ~ 25 kb upstream of the TSS. Intact IL-27 signalling was an essential requirement for these persistent epigenetic changes in memory CD4+ Tcells. We identified CREB1 as a transcription factor binding the Il10 active enhancer, and we showed that the ability of IL-27 to promote IL-10 expression was dependent on the histone acetyl transferase activity of the CREB1 complex member, p300. Together our data provide mechanistic insight into the action of IL-27 in regulating an immune response. We suggest that infection-induced cytokine signals direct epigenetic changes that moderate cytokine output in response to T cell receptor stimulation, regulating immune activity at sites of infection.
2022-12-31 | GSE135247 | 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:Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection. Lung TRM can be generated in response to respiratory infection or vaccination, however, the molecular pathways involved in CD4+TRM establishment have not been defined. Here, we performed transcriptional profiling of influenza-specific lung CD4+TRM following influenza infection to identify pathways implicated in CD4+TRM generation and homeostasis. Lung CD4+TRM displayed a unique transcriptional profile distinct from spleen memory, including up-regulation of a gene network induced by the transcription factor IRF4, a known regulator of effector T cell differentiation.
2020-09-01 | GSE137386 | 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.
2015-05-14 | GSE60186 | GEO
Project description:Memory antigen-specific CD4+ T cells against Chlamydia trachomatis are necessary for protection against secondary genital tract infection. While it is known that naïve antigen-specific CD4+ T cells can traffic to the genital tract in an antigen-specific manner, these T cells are not protective during primary infection. Here, we sought to compare the differences between memory and naïve antigen-specific CD4+ T cells in the same mouse following secondary infection using transgenic CD4+ T cells (NR1 T cells). Using RNA sequencing, we found that there were subtle but distinct differences between these two T cell populations. Naïve NR1 T cells significantly upregulated cell cycle genes and were more proliferative than memory NR1 T cells in the draining lymph node. In contrast, memory NR1 T cells were more activated than naïve NR1 T cells and were enriched in the genital tract. Together, our data provide insight into the differences between memory and naïve antigen-specific CD4+ T cells during C. trachomatis infection.
2020-05-01 | GSE146265 | GEO