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KMID : 0364820130490040301
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Korean Journal of Microbiology
2013 Volume.49 No. 4 p.301 ~ p.308
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PD-1 Expression in LPS-Induced Raw264.7 Cells Is Regulated via Co-activation of Transcription Factor NF-κB and IRF-1
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Choi Eun-Kyoung
Lee Soo-Woon
Lee Soo-Woong
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Abstract
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Programmed Death-1 (PD-1) is one of the important immune-inhibitory molecules which was expressed in T cells, B
cells, NKT cells, and macrophages activated by various immune activating factors. Lipopolysaccharide (LPS), the
major component of the outer membrane of Gram-negative bacteria, is one of the crucial immunogens for PD-1
expression. However, there are only a few reports on the expression mechanisms of PD-1 in innate immune cells. In
this study, we investigate the expression mechanisms of PD-1 in LPS-stimulated Raw264.7 cell lines by RT-PCR,
Western Blot, flow cytometry as well as ChIP assay and co-immunoprecipitation. When Raw264.7 cells were
stimulated with LPS, PD-1 expression was greatly up-regulated via PI3K and p38 signaling. Primary macrophages
isolated from LPS-injected mice were also shown the increased expression of PD-1. In promoter assay, NF-κB and
IRF-1 binding regions in mouse PD-1 promoter are important for PD-1 expression. We also found that the
co-activation of NF-κB and IRF-1 is indispensable for the maximum PD-1 expression. These results indicate that the
modulation of PD-1 expressed in innate immune cells could be a crucial for the disease therapy such as LPS-induced
mouse sepsis model.
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KEYWORD
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IRF-1, lipopolysaccharide, NF-κB, programmed Death-1, Raw264.7
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