Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from primary and secondary CD4 T cell effectors responding towards influenza A virus infection

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Susan Swain

PROVIDER: E-GEOD-40230 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Memory CD4+ T-cell-mediated protection depends on secondary effectors that are distinct from and superior to primary effectors.

Strutt Tara M TM McKinstry K Kai KK Kuang Yi Y Bradley Linda M LM Swain Susan L SL

Proceedings of the National Academy of Sciences of the United States of America 20120827 38

Whether differences between naive cell-derived primary (1°) and memory cell-derived secondary (2°) CD4(+) T-cell effectors contribute to protective recall responses is unclear. Here, we compare these effectors directly after influenza A virus infection. Both develop with similar kinetics, but 2° effectors accumulate in greater number in the infected lung and are the critical component of memory CD4(+) T-cell-mediated protection against influenza A virus, independent of earlier-acting memory-cell ...[more]

PMID: 22927425

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Project description:Tumors express a wide variety of both mutated and non-mutated antigens. Whether these tumor antigens are broadly recognized as âselfâ or âforeignâ by the immune system is currently unclear. Using an autochthonous prostate cancer model in which hemagglutinin (HA) is specifically expressed in the tumor (ProHA x TRAMP mice), as well as an analogous model wherein HA is expressed in normal tissues as a model self-antigen (C3HAHigh), we examined the transcriptional profile of CD4 T cells undergoing antigen-specific division. Consistent with our previous data, transfer of antigen-specific CD4 T cells into C3HAHigh resulted in a functionally inactivated CD4 T cell profile. Conversely, adoptive transfer of an identical CD4 T cell population into ProHA x TRAMP resulted in the induction of a regulatory phenotype (Treg) both at the transcriptional and functional level. Interestingly, this Treg skewing was a property of even early-stage tumors, suggesting Treg induction as an important tolerance mechanism during tumor development. The goal of this microarray is to detail the transcriptional profile differences between CD4 T cells that recognize their cognate antigen in the context of tumor (ProHA x TRAMP model) or self-antigen recognition (C3HA) or viral-antigen recognition (VaccHA) models or unprimed naÃ¯ve state (Nontransgenic). The comparison contains both upregulated and downregulated transcripts. Experiment Overall Design: TCR transgenic CD4 T cells specific for hemagglutinin (HA) were adoptively transferred into tumor-antigen recognition model (ProHA x TRAMP), Self-antigen recognition model (C3HA), viral-antigen recognition model (VaccHA), and naÃ¯ve control (Nontrangenic). Divided (CFSE diluted) CD4 T cells were sorted by FACS, RNA was extracted, and biological replicated were hybridized to an Affymetrix Mouse 430 Plus 2 expression array, followed by interrogation with an Affymetrix GeneChip Scanner 3000. RMA normalization was employed to identify differentially expressed transcripts.

Dataset Information

Expression data from primary and secondary CD4 T cell effectors responding towards influenza A virus infection

Publications

Memory CD4+ T-cell-mediated protection depends on secondary effectors that are distinct from and superior to primary effectors.

Similar Datasets

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