Signal integration between IFNγ and TLR signalling pathways in macrophages

被引:237
作者
Schroder, Kate
Sweet, Matthew J.
Hume, David A.
机构
[1] Univ Queensland, Inst Mol Biosci, Special Res Ctr Funct & Appl Gen, Brisbane, Qld 4072, Australia
[2] Univ Queensland, Sch Mol & Microbial Sci, Brisbane, Qld 4072, Australia
关键词
CpG DNA; endotoxin tolerance; interferon; lipopolysaccharide; nitric oxide; STAT1; toll-like receptor;
D O I
10.1016/j.imbio.2006.05.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Macrophages are major effector cells of the innate immune system, and appropriate regulation of macrophage function requires the integration of multiple signalling inputs derived from the recognition of host factors (e.g. interferon-gamma/IFN gamma) and pathogen products (e.g. toll-like receptor/TLR agonists). The profound effects of IFN gamma pre-treatment ("priming") on TLR-induced macrophage activation have long been recognised, but many of the mechanisms underlying the priming phenotype have only recently been identified. This review summarises the known mechanisms of integration between the IFN gamma and TLR signalling pathways. Synergy occurs at multiple levels, ranging from signal recognition to convergence of signals at the promoters of target genes. In particular, the cross-talk between the IFN gamma and LPS and CpG DNA signalling pathways is discussed. (c) 2006 Elsevier GmbH. All rights reserved.
引用
收藏
页码:511 / 524
页数:14
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