![]() ![]() Financial support from the National Institutes of Health (Bethesda, Maryland, United States) is acknowledged.Ĭompeting interests: The authors have declared that no competing interests exist. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.įunding: This work was supported by CNRS, the Ministère de l'Education Nationale de la Recherche et de la Technologie, the Fondation pour le Recherche Médicale and the Agence National pour la Recherche (ACI jeunes Chercheurs and IUF to JR). Received: DecemAccepted: JanuPublished: February 24, 2006Ĭopyright: © 2006 Bischoff et al. PLoS Pathog 2(2):Įditor: David Schneider, Stanford University, United States of America Their results suggest that these proteins are required in the larval gut to negatively regulate the immune response, thus preventing bacterially induced developmental defects and death.Ĭitation: Bischoff V, Vignal C, Duvic B, Boneca IG, Hoffmann JA, Royet J (2006) Downregulation of the Drosophila Immune Response by Peptidoglycan-Recognition Proteins SC1 and SC2. Here, the authors investigate in vivo data on the role of Drosophila PGRPs with enzymatic activity. The contribution of PGRPs which have maintained enzymatic activity to host defense has remained elusive so far. It has been shown previously that some PGRPs have lost this enzymatic activity and function as sensors of bacteria upstream of the Drosophila immune pathways. PGRPs are evolutionarily conserved molecules derived from enzymes that cleave bacterial peptidoglycan. Using the fruit fly as a model, evidence is presented that such an immuno-modulation is also essential in invertebrates and is mediated by peptidoglycan-recognition proteins (PGRPs). However, excessive or inappropriate inflammation can be harmful or event fatal. Responses that are delayed or of insufficient vigor can lead to a failure to control infection. It has long been known that the mammalian immune response needs to be kept under tight control. We further show that a strict control of IMD-pathway activation is essential to prevent bacteria-induced developmental defects and larval death. Our data suggest that these proteins act in the larval gut to prevent activation of this pathway following bacterial ingestion. We observed that PGRP-SC1/2–depleted flies present a specific over-activation of the IMD (immune deficiency) signaling pathway after bacterial challenge. Using an RNA-interference approach, we addressed the function of two PGRPs with amidase activity in the Drosophila immune response. However, the contribution of these amidase PGRPs to host defense in vivo has remained elusive so far. Other PGRP family members, such as Drosophila PGRP-SC1 or mammalian PGRP-L, have conserved the amidase function and are able to cleave peptidoglycan in vitro. Several Drosophila PGRPs have lost this enzymatic activity and serve as microbe sensors through peptidoglycan recognition. Peptidoglycan-recognition proteins (PGRPs) are evolutionarily conserved molecules that are structurally related to bacterial amidases.
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