期刊
NATURE IMMUNOLOGY
卷 14, 期 6, 页码 593-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2576
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资金
- US National Institutes of Health [U19 AI83022, U19 AI82630, R01 AI66215, R01 AI46719]
- Department of Microbiology and Immunology
- Biotechnology and Biological Sciences Research Council
- Medical Research Council
- BBSRC [BB/J00152X/1, BBS/E/B/000C0407, BBS/E/B/000C0409] Funding Source: UKRI
- MRC [G1001068] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C206, BB/J00152X/1, BBS/E/B/000C0407, BBS/E/B/000C0409, BBS/E/B/0000C207] Funding Source: researchfish
- Medical Research Council [G1001068] Funding Source: researchfish
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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