The transcription factor Zbtb32 controls the proliferative burst of virus-specific natural killer cells responding to infection
Copyright policy )The transcription factor Zbtb32 controls the proliferative burst of virus-specific natural killer cells responding to infection
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) was essential for the proliferative burst and protective capacity of virus-specific NK cells. Signals from proinflammatory cytokines were both necessary and sufficient to induce high expression of Zbtb32 in NK cells. Zbtb32 facilitated NK cell proliferation during infection by antagonizing the anti-proliferative factor Blimp-1 (Prdm1). Our data support a model in which Zbtb32 acts as a cellular 'hub' through which proinflammatory signals instruct a 'proliferation-permissive' state in NK cells, thereby allowing their prolific expansion in response to viral infection.
- Chiba University Japan
- Memorial Sloan Kettering Cancer Center United States
Inflammation, Mice, Knockout, Muromegalovirus, Cell Survival, Herpesviridae Infections, Adaptive Immunity, Lymphocyte Activation, Killer Cells, Natural, Mice, Inbred C57BL, Repressor Proteins, Mice, Animals, Cytokines, Positive Regulatory Domain I-Binding Factor 1, Immunologic Memory, Cell Proliferation, Transcription Factors
Inflammation, Mice, Knockout, Muromegalovirus, Cell Survival, Herpesviridae Infections, Adaptive Immunity, Lymphocyte Activation, Killer Cells, Natural, Mice, Inbred C57BL, Repressor Proteins, Mice, Animals, Cytokines, Positive Regulatory Domain I-Binding Factor 1, Immunologic Memory, Cell Proliferation, Transcription Factors
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