期刊
IMMUNITY
卷 34, 期 5, 页码 715-728出版社
CELL PRESS
DOI: 10.1016/j.immuni.2011.04.014
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资金
- National Institutes of Health [HL72952, HL75427, HL76754, HL086548, HL084154, P01 HL048743, HL097023, HL078806, HL087595, HL088740, HL086614, HL094660, GM064619, HL100474]
- Robert Wood Johnson/Harold Amos Medical Faculty Development grant
- Dominic Visconsi Scholar Award
- American Heart Association [0725297B, 09POST2060203]
- Sankyo Foundation of Life Science
- Kanae Foundation for the Promotion of Medical Science
Precise control of myeloid cell activation is required for optimal host defense. However, this activation process must be under exquisite control to prevent uncontrolled inflammation. Herein, we identify the Kruppel-like transcription factor 2 (KLF2) as a potent regulator of myeloid cell activation in vivo. Exposure of myeloid cells to hypoxia and/or bacterial products reduced KLF2 expression while inducing hypoxia inducible factor-1 alpha (HIF-1 alpha), findings that were recapitulated in human septic patients. Myeloid KLF2 was found to be a potent inhibitor of nuclear factor-kappaB (NF-kappa B)-dependent HIF-1 alpha. transcription and, consequently, a critical determinant of outcome in models of polymicrobial infection and endotoxemia. Collectively, these observations identify KLF2 as a tonic repressor of myeloid cell activation in vivo and an essential regulator of the innate immune system.
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