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We found upregulation of expression of the microRNA miR-155 in primary effector and effector memory CD8(+) T cells, but low miR-155 expression in naive and central memory cells. Antiviral CD8(+) T cell responses and viral clearance were impaired in miR-155-deficient mice, and this defect was intrinsic to CD8(+) T cells, as miR-155-deficient CD8(+) T cells mounted greatly diminished primary and memory responses. Conversely, miR-155 overexpression augmented antiviral CD8(+) T cell responses in vivo. Gene-expression profiling showed that miR-155-deficient CD8(+) T cells had enhanced type I interferon signaling and were more susceptible to interferon's antiproliferative effect. Inhibition of the type I interferon-associated transcription factors STAT1 or IRF7 resulted in enhanced responses of miR-155-deficient CD8(+) T cells in vivo. We have thus identified a previously unknown role for miR-155 in regulating responsiveness to interferon and CD8(+) T cell responses to pathogens in vivo.

Original publication

DOI

10.1038/ni.2576

Type

Journal article

Journal

Nat Immunol

Publication Date

06/2013

Volume

14

Pages

593 - 602

Keywords

Animals, CD8-Positive T-Lymphocytes, Cell Proliferation, Flow Cytometry, Gene Expression Profiling, Gene Regulatory Networks, Immunoblotting, Immunologic Memory, Interferon Regulatory Factor-7, Interferons, Mice, Mice, Inbred C57BL, Mice, Knockout, MicroRNAs, Oligonucleotide Array Sequence Analysis, Orthomyxoviridae, Orthomyxoviridae Infections, RNA Interference, Reverse Transcriptase Polymerase Chain Reaction, STAT1 Transcription Factor, Signal Transduction, Suppressor of Cytokine Signaling 1 Protein, Suppressor of Cytokine Signaling Proteins