%0 Journal Article
%T Promoting effect of IFN-γ on the expression of LPS-induced IL-12 p40 and p35 mRNA in murine suppressor macrophages<br>
%A QI Jie
%A ZHANG Jinsong
%A FENG Weiguo
%A LUO Xiangdong
%A LI Changlin ZHANG Zongliang
%A <br>
%J 中国科学C辑(英文版)
%D 2000
%I Springer
%X We detected the expression of IL-12 p40/p35 mRNA by semi-quantitative RT-PCR and silver staining, and studied the molecular interaction between the IL-12 expression and the NF-eB activation induced by LPS and IFN-γ/LPS in murine peritoneal suppressor macrophages (MPSMs). It was found that IFN-γ strongly enhanced the LPS-induced IL-12 p40 and p35 mRNA expression. Both p40 and p35 mRNA levels were approximately equal. IFN-a also greatly promoted the LPS-induced secretion of IL-12 p70 in MPSMs. The Proteasome Inhibitor I (PSI) could block the expression of IL-12 p40 and p35 mRNA, and the degradation of IκBα induced by LPS or LPS/IFN-γ. EMSA showed that LPS could augment the NF-κB binding activity to p40 promoter DNA. However, IFN-γ could neither enhance the LPS-induced NF-κB activity nor promote the degradation of IκBα. Taken together, the data suggest: (i) IFN-γ/LPS could strongly induce the expression of IL-12 p40 and p35 mRNA; both the expression levels were equal; this phenomenon coincided with the high-level secretion of IL-12 p70 induced by IFN-γ/LPS; (ii) NF-κB signal pathway is essential for IFN-γ/LPS to induce IL-12 mRNA expression; (iii) by blocking the degradation of IκB, the PSI suppresses the IL-12 p40/p35 mRNA expression induced by LPS and IFN-γ/LPS; (iv) NF-κB signal may not be involved in the mechanism by which IFN-γ enhanced the expression of the LPS-induced IL-12 p40/p35 mRNA. The first two authors contributed equally to this work.
%K IL-12 p40/p35
%K LPS
%K suppressor macrophage
%K IFN-γ
%K NF-κ
%K B<br>
%U http://www.alljournals.cn/get_abstract_url.aspx?pcid=90BA3D13E7F3BC869AC96FB3DA594E3FE34FBF7B8BC0E591&jid=180CF3A72E750F3261A8A60EDC957784&aid=75EBDE30B9C4568F&yid=9806D0D4EAA9BED3&vid=BE33CC7147FEFCA4&iid=B31275AF3241DB2D&sid=C2053D4E59904B8A&eid=4964C30D71DF45FF&journal_id=1674-7305&journal_name=ScienceChina.Lifesciences&referenced_num=0&reference_num=15