| Literature DB >> 24360958 |
Obinna Chijioke1, Anne Müller1, Regina Feederle2, Mario Henrique M Barros3, Carsten Krieg4, Vanessa Emmel5, Emanuela Marcenaro6, Carol S Leung1, Olga Antsiferova1, Vanessa Landtwing1, Walter Bossart7, Alessandro Moretta6, Rocio Hassan5, Onur Boyman4, Gerald Niedobitek3, Henri-Jacques Delecluse2, Riccarda Capaul7, Christian Münz8.
Abstract
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.Entities:
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Year: 2013 PMID： 24360958 PMCID： PMC3895765 DOI： 10.1016/j.celrep.2013.11.041
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423