期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 12, 页码 8011-8019出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.12.8011
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LPS is the known component of bacterial pathogens that stimulates a number of proinflammatory factors. However, the mechanism of the induction of these factors by LPS has not been fully elucidated. We show here that LPS induces retinoic acid-inducible gene-I (RIG-I) in vitro and in vivo as a result from autocrine secretion of IFN-beta in macrophages. TIR-domain-containing adapter-inducing IFN-beta-deficient mouse embryo fibroblast (trif(-/-)) fail to show expression of RIG-I following LPS stimulation. Interference of RIG-I expression short interfering RNA represses the expression of LPS-induced TNF-alpha, whereas over-expression of RIG-I leads to the activation of TNF-alpha promoter and the induction of TNF-alpha expression. LPS- and IFN-beta-induced TNF-alpha are suppressed in RIG-I-deficient mouse embryo fibroblasts (rig(-/-)). Thus, RIG-I plays a key role in the expression of TNF-alpha in macropbages in response to LPS stimulation, mainly for the late phase LPS-induced expression of TNF-alpha.
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