Transcriptomics

Dataset Information

36

Expression data from WT and IL-2 secondary CD4 T cell effectors responding towards infuenza A virus infection


ABSTRACT: 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.

ORGANISM(S): Mus musculus  

SUBMITTER: Karl K McKinstry  Tara M Strutt   Susan L Swain    

PROVIDER: E-GEOD-60186 | ArrayExpress | 2015-05-22

SECONDARY ACCESSION(S): GSE60186PRJNA257695

REPOSITORIES: GEO, ArrayExpress

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Publications

Effector CD4 T-cell transition to memory requires late cognate interactions that induce autocrine IL-2.

McKinstry K Kai KK   Strutt Tara M TM   Bautista Bianca B   Zhang Wenliang W   Kuang Yi Y   Cooper Andrea M AM   Swain Susan L SL  

Nature communications 20141105


It is unclear how CD4 T-cell memory formation is regulated following pathogen challenge, and when critical mechanisms act to determine effector T-cell fate. Here, we report that following influenza infection most effectors require signals from major histocompatibility complex class II molecules and CD70 during a late window well after initial priming to become memory. During this timeframe, effector cells must produce IL-2 or be exposed to high levels of paracrine or exogenously added IL-2 to su  ...[more]

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