The transcription factor Zbtb32 controls the proliferative burst of virus-specific natural killer cells responding to infection.
The transcription factor Zbtb32 controls the proliferative burst of virus-specific natural killer cells responding to infection.
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Natural Killer (NK) cells are innate lymphocytes that exhibit many features of adaptive immunity including clonal proliferation and long-lived memory. Here we demonstrate that the BTB-ZF transcription factor Zbtb32 (also known as ROG, FAZF, TZFP, and PLZP) is essential for the proliferative burst and protective capacity of virus-specific NK cells. Signals from proinflammatory cytokines are both necessary and sufficient to induce high Zbtb32 expression in NK cells. Mechanistically, we show that Zbtb32 facilitates NK cell proliferation during infection by antagonizing the anti-proliferative factor Blimp-1 (Prdm1). Taken together, our data support a model in which Zbtb32 acts as a cellular “hub” through which pro-inflammatory signals instruct a “proliferation-permissive” state in NK cells, thereby allowing their prolific expansion in response to viral infection.
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影响因子:
30.5
作者:
通讯作者:
--
影响因子:
56.9
作者:
Brown, MG;Dokun, AO;Yokoyama, WM
通讯作者:
Yokoyama, WM
影响因子:
64.8
作者:
He, X;He, X;Kappes, DJ
通讯作者:
Kappes, DJ
影响因子:
32.4
作者:
Miaw, SC;Choi, A;Ho, IC
通讯作者:
Ho, IC
DOI:
10.4049/jimmunol.1004006
发表时间:
2011-09-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Beaulieu AM;Sant'Angelo DB
通讯作者:
Sant'Angelo DB