Dataset Information


MiR31 increases CD8 T cell sensitivity to type I interferon

ABSTRACT: We report that the microRNA (miR)-31 confers CD8 T cell sensitivity to type I interferon (IFN) stimulation following CD3/CD28 engagement. Method: miR31 WT and KO CD8 T cells were stimulated with anti-CD3/CD28 beads for two days, then maintained in 10ng/mL IL-2 for a further 5 days. CD8 T cells were then stimulated with 20ng/mL IFN-beta for 0, 4, or 18h. Total RNA was isolated at each time point and sequenced. Results: Prior to IFN-beta stimulation, miR-31 KO CD8 T cells had a slightly increased effector program (cytotoxic granzymes) and decreased inhibitory program (Mt1/Maf). Stimulation with IFN-beta further enhanced this difference increasing a number of granzymes, Prf1 and Spp1 whilst also decreasing inhibitory genes (Mt1, Mt2, Maf, Ptger2). Conclusion: This study shows that miR-31 may lead to decreased effector function and increased inhibitory programs in CD8 T cells during chronic viral infections, in particular due to continued type I interferon stimulation. Overall design: RNA profiles of miR31 WT or KO CD8 T cells were generated in triplicate following a 7 day TCR/IL-2 stimulation followed by 0, 4, or 18 hours IFN-beta stimulation.

INSTRUMENT(S): Illumina NextSeq 500 (Mus musculus)

SUBMITTER: Kai W Wucherpfennig  

PROVIDER: GSE98615 | GEO | 2017-05-07



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During infection, antigen-specific T cells undergo tightly regulated developmental transitions controlled by transcriptional and post-transcriptional regulation of gene expression. We found that the microRNA miR-31 was strongly induced by activation of the T cell antigen receptor (TCR) in a pathway involving calcium and activation of the transcription factor NFAT. During chronic infection with lymphocytic choriomeningitis virus (LCMV) clone 13, miR-31-deficent mice recovered from clinical diseas  ...[more]

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