| Literature DB >> 23601686 |
Jan C Dudda1, Bruno Salaun, Yun Ji, Douglas C Palmer, Gwennaelle C Monnot, Estelle Merck, Caroline Boudousquie, Daniel T Utzschneider, Thelma M Escobar, Rachel Perret, Stefan A Muljo, Michael Hebeisen, Nathalie Rufer, Dietmar Zehn, Alena Donda, Nicholas P Restifo, Werner Held, Luca Gattinoni, Pedro Romero.
Abstract
MicroRNAs (miRNAs) regulate the function of several immune cells, but their role in promoting CD8(+) T cell immunity remains unknown. Here we report that miRNA-155 is required for CD8(+) T cell responses to both virus and cancer. In the absence of miRNA-155, accumulation of effector CD8(+) T cells was severely reduced during acute and chronic viral infections and control of virus replication was impaired. Similarly, Mir155(-/-) CD8(+) T cells were ineffective at controlling tumor growth, whereas miRNA-155 overexpression enhanced the antitumor response. miRNA-155 deficiency resulted in accumulation of suppressor of cytokine signaling-1 (SOCS-1) causing defective cytokine signaling through STAT5. Consistently, enforced expression of SOCS-1 in CD8(+) T cells phenocopied the miRNA-155 deficiency, whereas SOCS-1 silencing augmented tumor destruction. These findings identify miRNA-155 and its target SOCS-1 as key regulators of effector CD8(+) T cells that can be modulated to potentiate immunotherapies for infectious diseases and cancer.Entities:
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Year: 2013 PMID: 23601686 PMCID: PMC3788592 DOI: 10.1016/j.immuni.2012.12.006
Source DB: PubMed Journal: Immunity ISSN: 1074-7613 Impact factor: 31.745