MicroRNA-155 Is Required for Effector CD8(+) T Cell Responses to Virus Infection and Cancer.

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Download: 0_23601686_Postprint.pdf (1649.96 [Ko])
State: Public
Version: author
Serval ID
serval:BIB_C465F0F1D8F8
Type
Article: article from journal or magazin.
Collection
Publications
Title
MicroRNA-155 Is Required for Effector CD8(+) T Cell Responses to Virus Infection and Cancer.
Journal
Immunity
Author(s)
Dudda J.C., Salaun B., Ji Y., Palmer D.C., Monnot G.C., Merck E., Boudousquie C., Utzschneider D.T., Escobar T.M., Perret R., Muljo S.A., Hebeisen M., Rufer N., Zehn D., Donda A., Restifo N.P., Held W., Gattinoni L., Romero P.
ISSN
1097-4180 (Electronic)
ISSN-L
1074-7613
Publication state
Published
Issued date
2013
Peer-reviewed
Oui
Volume
38
Number
4
Pages
742-753
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
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.
Pubmed
Web of science
Open Access
Yes
Create date
14/05/2013 9:38
Last modification date
20/08/2019 16:39
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