C/EBPβ is required for 'emergency' granulopoiesis

被引:341
作者
Hirai, Hideyo
Zhang, Pu
Dayaram, Tajhal
Hetherington, Christopher J.
Mizuno, Shin-ichi
Imanishi, Jiro
Akashi, Koichi
Tenen, Daniel G. [1 ]
机构
[1] Harvard Univ, Inst Med, Boston, MA 02115 USA
[2] Harvard Univ, Stem Cell Inst, Boston, MA 02115 USA
[3] Kyoto Prefectural Univ Med, Dept Microbiol, Kyoto 602, Japan
[4] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA
[5] Kyushu Univ Hosp, Ctr Cellular & Mol Med, Fukuoka 8120034, Japan
关键词
D O I
10.1038/ni1354
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
During 'emergency' situations such as infections, host defense requires rapid mobilization of bone marrow granulocyte progenitors. 'Steady-state' granulopoiesis is absolutely dependent on the C/EBP alpha transcription factor, but the transcriptional mechanisms underlying emergency granulopoiesis remain unclear. Here we show that large numbers of granulocytes were generated from C/EBP alpha-deficient progenitors after cytokine stimulation in vivo. Cytokine treatment or fungal infection induced upregulation of C/EBP beta but not C/EBP alpha or C/EBP epsilon transcripts in granulocyte progenitors, and C/EBP beta-deficient progenitors showed decreased emergency-induced granulopoiesis in vitro and in vivo. C/EBPb inhibited proliferation less severely than did C/EBP alpha. These data suggest a critical function for C/EBP beta in emergency granulopoiesis, which demands both differentiation and proliferation of granulocyte precursors.
引用
收藏
页码:732 / 739
页数:8
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