Drosophila melanogaster innate immunity:: an emerging role for peptidoglycan recognition proteins in bacteria detection

被引:19
作者
Royet, J [1 ]
机构
[1] Univ Strasbourg, Inst Biol Mol & Cellulaire, CNRS Reponse Immunitaire Invertebres, UPR 9022, F-67084 Strasbourg, France
关键词
innate immunity; Drosophila melanogaster; Toll; PGRP; antimicrobial peptides; peptidoglycan;
D O I
10.1007/s00018-003-3243-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Over the past years, parallel studies conducted in mammals and flies have emphasized the existence of common mechanisms regulating the vertebrate and invertebrate innate immune systems. This culminated in the discovery of the central role of the Toll pathway in Drosophila immunity and in the implication of Toll-like receptors (TLRs)/interleukin-1(IL-1) in the mammalian innate immune response. In spite of clear similarities, such as shared intracellular pathway components, important divergences are expected between the two groups, whose last common ancestor lived more than half a billion years ago. The most obvious discrepancies lie in the mode of activation of the signalling receptors by microorganisms. In mammals, TLRs are part of protein complexes which directly recognize microbe-associated patterns, whereas Drosophila Toll functions like a classical cytokine receptor rather than a pattern recognition receptor. Recent studies demonstrate that members of the evolutionarily conserved peptidoglycan recognition protein family play an essential role in microbial sensing during immune response of Drosophila.
引用
收藏
页码:537 / 546
页数:10
相关论文
共 105 条
[21]   Notch signaling controls lineage specification during Drosophila larval hematopoiesis [J].
Duvic, B ;
Hoffmann, JA ;
Meister, M ;
Royet, J .
CURRENT BIOLOGY, 2002, 12 (22) :1923-1927
[22]   Defect in neutrophil killing and increased susceptibility to infection with-nonpathogenic gram-positive bacteria in peptidoglycan recognition protein-S (PGRP-S)-deficient mice [J].
Dziarski, R ;
Platt, KA ;
Gelius, E ;
Steiner, H ;
Gupta, D .
BLOOD, 2003, 102 (02) :689-697
[23]   Interactions between the cellular and humoral immune responses in Drosophila [J].
Elrod-Erickson, M ;
Mishra, S ;
Schneider, D .
CURRENT BIOLOGY, 2000, 10 (13) :781-784
[25]   KAPPA-B-LIKE MOTIFS REGULATE THE INDUCTION OF IMMUNE GENES IN DROSOPHILA [J].
ENGSTROM, Y ;
KADALAYIL, L ;
SUN, SC ;
SAMAKOVLIS, C ;
HULTMARK, D ;
FAYE, I .
JOURNAL OF MOLECULAR BIOLOGY, 1993, 232 (02) :327-333
[26]  
Fernandez NQ, 2001, DEVELOPMENT, V128, P2963
[27]   Collaborative induction of inflammatory responses by dectin-1 and toll-like receptor 2 [J].
Gantner, BN ;
Simmons, RM ;
Canavera, SJ ;
Akira, S ;
Underhill, DM .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 197 (09) :1107-1117
[28]   A mammalian peptidoglycan recognition protein with N-acetylmuramoyl-L-alanine amidase activity [J].
Gelius, E ;
Persson, C ;
Karlsson, J ;
Steiner, H .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 306 (04) :988-994
[29]   Drosophila immune deficiency (IMD) is a death domain protein that activates antibacterial defense and can promote apoptosis [J].
Georgel, P ;
Naitza, S ;
Kappler, C ;
Ferrandon, D ;
Zachary, D ;
Swimmer, C ;
Kopczynski, C ;
Duyk, G ;
Reichart, JM ;
Hoffmann, JA .
DEVELOPMENTAL CELL, 2001, 1 (04) :503-514
[30]   Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection [J].
Girardin, SE ;
Boneca, IG ;
Viala, J ;
Chamaillard, M ;
Labigne, A ;
Thomas, G ;
Philpott, DJ ;
Sansonetti, PJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (11) :8869-8872