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Whole genome mRNA analysis of wild-type and Id2-deficient virus-specific CD8+ T cells after influenza infection

ABSTRACT: The transcription factor Inhibitor of DNA binding 2 (Id2) modulates T cell fate decisions but the molecular mechanism underpinning this regulation is unclear. Here, using whole genome mRNA analysis we show that loss of Id2 programs CD8+ T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. Our findings reveal that the Id2-E2A axis orchestrates T cell differentiation through the induction or repression of downstream transcription factors essential for effector and memory T cell differentiation. Wild-type and Id2fl/flLckCre+ DbNP366-specific CD8+ T cells were isolated from the spleen of PR8-primed/HKx31-infected Ly5.2+Id2fl/flLckCre+:Ly5.1+ mixed bone marrow chimeric mice ten days after intranasal influenza infection and analysed by whole genome mRNA analysis. Three biological replicates of each genotype were subjected to microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Moshe Olshansky 

PROVIDER: E-GEOD-44141 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Id2-mediated inhibition of E2A represses memory CD8+ T cell differentiation.

Masson Frederick F   Minnich Martina M   Olshansky Moshe M   Bilic Ivan I   Mount Adele M AM   Kallies Axel A   Speed Terence P TP   Busslinger Meinrad M   Nutt Stephen L SL   Belz Gabrielle T GT  

Journal of immunology (Baltimore, Md. : 1950) 20130327 9

The transcription factor inhibitor of DNA binding (Id)2 modulates T cell fate decisions, but the molecular mechanism underpinning this regulation is unclear. In this study we show that loss of Id2 cripples effector differentiation and instead programs CD8(+) T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. We demonstrate that Id2 restrains CD8(+) T cell memory differentiation by inhibiting E2A-mediated direct activation of Tcf7 and that Id2 expression level mirrors  ...[more]

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