Pattern-recognition receptors in plant innate immunity

2008 ◽  
Vol 20 (1) ◽  
pp. 10-16 ◽  
Author(s):  
Cyril Zipfel
2011 ◽  
Vol 108 (2) ◽  
pp. 235-248 ◽  
Author(s):  
Yury I. Miller ◽  
Soo-Ho Choi ◽  
Philipp Wiesner ◽  
Longhou Fang ◽  
Richard Harkewicz ◽  
...  

2016 ◽  
Vol 59 (9) ◽  
pp. 878-888 ◽  
Author(s):  
Lei Li ◽  
Yufei Yu ◽  
Zhaoyang Zhou ◽  
Jian-Min Zhou

2016 ◽  
Vol 90 (13) ◽  
pp. 6022-6035 ◽  
Author(s):  
Serena Vegna ◽  
Damien Gregoire ◽  
Marie Moreau ◽  
Patrice Lassus ◽  
David Durantel ◽  
...  

ABSTRACTHepatitis C virus (HCV) triggers innate immunity signaling in the infected cell. Replication of the viral genome is dispensable for this phenotype, and we along with others have recently shown that NS5B, the viral RNA-dependent RNA polymerase, synthesizes double-stranded RNA (dsRNA) from cellular templates, thus eliciting an inflammatory response, notably via activation of type I interferon and lymphotoxin β. Here, we investigated intracellular signal transduction pathways involved in this process. Using HepaRG cells, a model that largely recapitulates thein vivocomplexities of the innate immunity receptor signaling, we have confirmed that NS5B triggered increased expression of the canonical pattern recognition receptors (PRRs) specific for dsRNA, namely, RIG-I, MDA5, and Toll-like receptor 3 (TLR3). Unexpectedly, intracellular dsRNA also led to accumulation of NOD1, a receptor classically involved in recognition of bacterial peptidoglycans. NOD1 activation, confirmed by analysis of its downstream targets, was likely due to its interaction with dsRNA and was independent of RIG-I and mitochondrial antiviral signaling protein (MAVS/IPS-1/Cardif/VISA) signaling. It is likely to have a functional significance in the cellular response in the context of HCV infection since interference with the NOD1 pathway severely reduced the inflammatory response elicited by NS5B.IMPORTANCEIn this study, we show that NOD1, a PRR that normally senses bacterial peptidoglycans, is activated by HCV viral polymerase, probably through an interaction with dsRNA, suggesting that NOD1 acts as an RNA ligand recognition receptor. In consequence, interference with NOD1-mediated signaling significantly weakens the inflammatory response to dsRNA. These results add a new level of complexity to the understanding of the cross talk between different classes of pattern recognition receptors and may be related to certain complications of chronic hepatitis C virus infection.


2010 ◽  
Vol 101 (2) ◽  
pp. 313-320 ◽  
Author(s):  
Tsukasa Seya ◽  
Hiroaki Shime ◽  
Takashi Ebihara ◽  
Hiroyuki Oshiumi ◽  
Misako Matsumoto

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Md. Murad Hossain ◽  
Mohd-Nor Norazmi

Tuberculosis, an infectious disease caused byMycobacterium tuberculosis(Mtb), remains a major cause of human death worldwide. Innate immunity provides host defense against Mtb. Phagocytosis, characterized by recognition of Mtb by macrophages and dendritic cells (DCs), is the first step of the innate immune defense mechanism. The recognition of Mtb is mediated by pattern recognition receptors (PRRs), expressed on innate immune cells, including toll-like receptors (TLRs), complement receptors, nucleotide oligomerization domain like receptors, dendritic cell-specific intercellular adhesion molecule grabbing nonintegrin (DC-SIGN), mannose receptors, CD14 receptors, scavenger receptors, and FCγreceptors. Interaction of mycobacterial ligands with PRRs leads macrophages and DCs to secrete selected cytokines, which in turn induce interferon-γ- (IFNγ-) dominated immunity. IFNγand other cytokines like tumor necrosis factor-α(TNFα) regulate mycobacterial growth, granuloma formation, and initiation of the adaptive immune response to Mtb and finally provide protection to the host. However, Mtb can evade destruction by antimicrobial defense mechanisms of the innate immune system as some components of the system may promote survival of the bacteria in these cells and facilitate pathogenesis. Thus, although innate immunity components generally play a protective role against Mtb, they may also facilitate Mtb survival. The involvement of selected PRRs and cytokines on these seemingly contradictory roles is discussed.


Immunity ◽  
2009 ◽  
Vol 30 (6) ◽  
pp. 789-801 ◽  
Author(s):  
Mathieu J.M. Bertrand ◽  
Karine Doiron ◽  
Katherine Labbé ◽  
Robert G. Korneluk ◽  
Philip A. Barker ◽  
...  

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