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Accepted (AM)Open Access (License Unspecified), Open
Journal article
The microRNA miR-155 controls CD8(+) T cell responses by regulating interferon signaling
Nature immunology, v 14(6), pp 593-602
01 Jun 2013
PMID: 23603793
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
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.
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Details
- Title
- The microRNA miR-155 controls CD8(+) T cell responses by regulating interferon signaling
- Creators
- Donald T. Gracias - Drexel UniversityErietta Stelekati - Drexel UniversityJennifer L. Hope - Drexel UniversityAlina C. Boesteanu - Drexel UniversityTravis A. Doering - University of PennsylvaniaJillian Norton - Drexel UniversityYvonne M. Mueller - Drexel UniversityJoseph A. Fraietta - Drexel UniversityE. John Wherry - University of PennsylvaniaMartin Turner - Babraham InstitutePeter D. Katsikis - Drexel University
- Publication Details
- Nature immunology, v 14(6), pp 593-602
- Publisher
- Springer Nature
- Number of pages
- 12
- Grant note
- P30CA016520 / NATIONAL CANCER INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI) G1001068 / Medical Research Council; UK Research & Innovation (UKRI); Medical Research Council UK (MRC); European Commission Department of Microbiology and Immunology BB/J00152X/1 / BBSRC; UK Research & Innovation (UKRI); Biotechnology and Biological Sciences Research Council (BBSRC) U19 AI83022; U19 AI82630; R01 AI66215; R01 AI46719 / US National Institutes of Health; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA BB/J00152X/1 / Biotechnology and Biological Sciences Research Council; UK Research & Innovation (UKRI); Biotechnology and Biological Sciences Research Council (BBSRC) Biotechnology and Biological Sciences Research Council; UK Research & Innovation (UKRI); Biotechnology and Biological Sciences Research Council (BBSRC) R01AI046719 / NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Allergy & Infectious Diseases (NIAID) Medical Research Council; UK Research & Innovation (UKRI); Medical Research Council UK (MRC); European Commission G1001068 / MRC; UK Research & Innovation (UKRI); Medical Research Council UK (MRC)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Microbiology and Immunology; Biology
- Web of Science ID
- WOS:000319107600012
- Scopus ID
- 2-s2.0-84878259075
- Other Identifier
- 991019168443504721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Immunology