期刊
PLOS PATHOGENS
卷 10, 期 8, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1004333
关键词
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资金
- Sassella Foundation [10/02, 11/02, 12/02]
- Cancer Research Switzerland [KFS-02652-08-2010, KFS-3234-08-2013]
- Association for International Cancer Research [11-0516]
- KFSPMS of the University of Zurich
- KFSPHLD of the University of Zurich
- Baugarten Foundation
- Sobek Foundation
- Fondation Acteria
- Wellcome Trust
- Leukaemia and Lymphoma Research
- Medical Research Council
- Swiss National Science Foundation [310030_143979, CRSII3_136241]
Epstein Barr virus (EBV) infection expands CD8(+) T cells specific for lytic antigens to high frequencies during symptomatic primary infection, and maintains these at significant numbers during persistence. Despite this, the protective function of these lytic EBV antigen-specific cytotoxic CD8(+) T cells remains unclear. Here we demonstrate that lytic EBV replication does not significantly contribute to virus-induced B cell proliferation in vitro and in vivo in a mouse model with reconstituted human immune system components (huNSG mice). However, we report a trend to reduction of EBV-induced lymphoproliferation outside of lymphoid organs upon diminished lytic replication. Moreover, we could demonstrate that CD8(+) T cells against the lytic EBV antigen BMLF1 can eliminate lytically replicating EBV-transformed B cells from lymphoblastoid cell lines (LCLs) and in vivo, thereby transiently controlling high viremia after adoptive transfer into EBV infected huNSG mice. These findings suggest a protective function for lytic EBV antigen-specific CD8(+) T cells against EBV infection and against virus-associated tumors in extra-lymphoid organs. These specificities should be explored for EBV-specific vaccine development.
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