Sensing infection in Drosophila:: Toll and beyond

被引：86

作者：

Ferrandon, D ^{[1
]}

Imler, JL ^{[1
]}

Hoffmann, JA ^{[1
]}

机构：

[1] CNRS, Inst Biol Mol & Cellulaire, UPR 9022, F-67084 Strasbourg, France

来源：

SEMINARS IN IMMUNOLOGY | 2004年 / 16卷 / 01期

关键词：

Toll; peptidoglycan recognition protein; gram-negative binding protein; beta-glucan recognition protein; pattern recognition receptor;

D O I：

10.1016/j.smim.2003.10.008

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Drosophila has evolved a potent immune system that is somewhat adapted to the nature of infections through the selective activation of either one of two NF-kappaB-like signalling pathways, the Toll and IMD (Immune deficiency) pathways. In contrast to the mammalian system, the Toll receptor does not act as a pattern recognition receptor (PRR) but as a cytokine receptor. The sensing of microbial infections is achieved by at least four PRRs that belong to two distinct families: the peptidoglycan recognition proteins (PGRPs) and the Gram-negative binding proteins (GNBPs)/beta-glucan recognition proteins (PGRPs). (C) 2003 Elsevier Ltd. All rights reserved.

引用

页码：43 / 53

页数：11

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