The interferon in TLR signaling: more than just antiviral

被引:151
作者
Hertzog, PJ [1 ]
O'Nei, LA
Hamilton, JA
机构
[1] Monash Univ, Monash Inst Reprod & Dev, Ctr Funct Genom & Human Dis, Clayton, Vic 3168, Australia
[2] Trinity Coll Dublin, Dept Biochem, Dublin 2, Ireland
[3] Univ Melbourne, Dept Med, Parkville, Vic 3052, Australia
关键词
D O I
10.1016/j.it.2003.08.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The Toll-like receptor (TLR) system is responsible for the recognition of infectious agents leading to initiation of the primary innate, and later adaptive, immune response. Genetic technologies have enabled the discovery of new factors involved in these systems, their genetic manipulation and the global analyses of their effects on gene expression. Furthermore, this increased understanding has resulted in the need to reassess our preconceptions about the functions of well-known molecules. For example, type I interferons (IFNs), which were discovered as antiviral proteins, are now known to be produced in response to TLR activation by many pathogens, including bacteria. Should we be surprised? Has the inflammatory response unexpectedly highjacked the body's antiviral system? Or are we too easily blinkered by preconceptions from how a compound was discovered?
引用
收藏
页码:534 / 539
页数:6
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