Journal
CELL REPORTS
Volume 5, Issue 6, Pages 1489-1498Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2013.11.041
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Funding
- National Cancer Institute [R01CA108609]
- Sassella Foundation [10/02, 11/02, 12/02]
- Cancer Research Switzerland [KFS-02652-08-2010]
- Association for International Cancer Research [11-0516]
- KFSP MS
- KFSP HLD of the University of Zurich
- Vontobel Foundation
- Baugarten Foundation
- EMDO Foundation
- Sobek Foundation
- Foundation Acteria
- Novartis
- Swiss National Science Foundation [310030_143979, CRSII3_136241]
- CNPq/INCT (Brazil) [CNPq 481294/2009-0, 573806/2008-0, FAPERJ-E-26/110.432/2010]
- Alexander von Humboldt Foundation
- postdoctoral fellowship of the Deutsche Forschungsgemeinschaft [CH 723/2-1]
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Primary infection with the human oncogenic Epstein-Barr virus (EBV) can result in infectious mononucleosis (IM), a self-limiting disease caused by massive lymphocyte expansion that predisposes for the development of distinct EBV-associated lymphomas. Why some individuals experience this symptomatic primary EBV infection, whereas the majority acquires the virus asymptomatically, remains unclear. Using a mouse model with reconstituted human immune system components, we show that depletion of human natural killer (NK) cells enhances IM symptoms and promotes EBV-associated tumorigenesis mainly because of a loss of immune control over lytic EBV infection. These data suggest that failure of innate immune control by human NK cells augments symptomatic lytic EBV infection, which drives lymphocyte expansion and predisposes for EBV-associated malignancies.
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