期刊
JOURNAL OF IMMUNOLOGY
卷 187, 期 7, 页码 3730-3737出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1101612
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资金
- Deutsche Forschungsgemeinschaft [TRR60, B4]
- Division of Intramural Research at the National Institute of Allergy and Infectious Diseases, National Institutes of Health
It was recently reported that inhibitory molecules such as programmed death-1 (PD-1) were upregulated on CD8(+) T cells during acute Friend retrovirus infection and that the cells were prematurely exhausted and dysfunctional in vitro. The current study confirms that most activated CD8(+) T cells upregulated expression of PD-1 during acute infection and revealed a dichotomy of function between PD-1(hi) and PD-1(lo) subsets. More PD-1(lo) cells produced antiviral cytokines such as IFN-gamma and TNF-alpha, whereas more PD-1(hi) cells displayed characteristics of cytotoxic effectors such as production of granzymes and surface expression of CD107a. Importantly, CD8(+) T cells mediated rapid in vivo cytotoxicity and were critical for control of acute Friend virus replication. Thus, direct ex vivo analyses and in vivo experiments revealed high CD8(+) T cell functionality and indicate that PD-1 expression during acute infection is not a marker of T cell exhaustion. The Journal of Immunology, 2011, 187: 3730-3737.
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