NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation

Cooney, Rachel; Baker, J. T.; Brain, Oliver; Danis, Bénédicte; Pichulik, Tica; Allan, Philip; Ferguson, David J. P.; Campbell, Barry J.; Jewell, D P; Simmons, Alison

doi:10.1038/nm.2069

Cited by 937 publications

(948 citation statements)

References 25 publications

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“…NLR triggering can enhance autophagy. NOD2 recognition of muramyldipeptide (a component of peptidoglycan) in human monocyte-derived DC enhances autophagy, as determined by fluorescence microscopy and LC3-I to LC3-II conversion (Cooney et al, 2010). In addition, triggering NOD1 in HeLa cells, and NOD2 in bone marrow-derived macrophages, enhances GFP-LC3 puncta, an observation suggestive of autophagy induction (Travassos et al, 2010).…”

Section: Regulation Of Autophagymentioning

confidence: 95%

Intersection of autophagy with pathways of antigen presentation

Patterson

Mintern

2012

Protein Cell

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Traditionally, macroautophagy (autophagy) is viewed as a pathway of cell survival. Autophagy ensures the elimination of damaged or unwanted cytosolic components and provides a source of cellular nutrients during periods of stress. Interestingly, autophagy can also directly intersect with, and impact, other major pathways of cellular function. Here, we will review the contribution of autophagy to pathways of antigen presentation. The autophagy machinery acts to modulate both MHCI and MHCII antigen presentation. As such autophagy is an important participant in pathways that elicit host cell immunity and the elimination of infectious pathogens.

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Section: Regulation Of Autophagymentioning

confidence: 95%

Intersection of autophagy with pathways of antigen presentation

Patterson

Mintern

2012

Protein Cell

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“…148,[163][164][165] This results in the expression of a range of inflammatory proteins, anti-bacterial proteins, activation of autophagy and antigen presentation. [166][167][168] Notably, RIP2 is required to mediate all of the in vivo host responses to MDP. 169 The ubiquitination of RIP2 is a critical step in mediating activation of these NOD2 pathways, especially activation of NFkB, 164,165 and a number of E3 ubiquitin ligases, including TRAF6, 164 cIAP and XIAP proteins [170][171][172] and ITCH 173 have been proposed to catalyse ubiquitination of RIP2.…”

Section: Rip2 and Nod Signallingmentioning

confidence: 99%

RIP kinases: key decision makers in cell death and innate immunity

et al. 2014

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“…Blockade of autophagy in DCs by chloroquine also delays the onset or reduces the severity of EAE [39] . DCs from patients with Crohn's disease with ATG16L1 and NOD2 variants are defective in antigen presentation [40] . The presentation of citrullinated peptides by DCs, macrophages, and thymic DCs is blocked by inhibition of autophagy with 3-methyladenine [41] .…”

Section: Autoreactive T-cell Regulation By Autophagymentioning

confidence: 99%

Role of autophagy in the pathogenesis of multiple sclerosis

Liang

2015

Neurosci. Bull.

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Autophagy plays an important role in maintaining the cellular homeostasis. One of its functions is to degrade unnecessary organelles and proteins for energy recycling or amino-acids for cell survival. Ablation of autophagy leads to neurodegeneration. Multiple sclerosis (MS), a permanent neurological impairment typical of chronic inflammatory demyelinating disorder, is an auto-immune disease of the central nervous system (CNS). Autophagy is tightly linked to the innate and adaptive immune systems during the autoimmune process, and several studies have shown that autophagy directly participates in the progress of MS or experimental autoimmune encephalomyelitis (EAE, a mouse model of MS). Dysfunction of mitochondria that intensively infl uences the autophagy pathway is one of the important factors in the pathogenesis of MS. Autophagy-related gene (ATG) 5 and immune-related GTPase M (IRGM) 1 are increased, while ATG16L2 is decreased, in T-cells in EAE and active relapsing-remitting MS brains. Administration of rapamycin, an inhibitor of mammalian target of rapamycin ( mTOR), ameliorates relapsing-remitting EAE. Infl ammation and oxidative stress are increased in MS lesions and EAE, but Lamp2 and the LC3-II/LC3-I ratio are decreased. Furthermore, autophagy in various glial cells plays important roles in regulating neuro-infl ammation in the CNS, implying potential roles in MS. In this review, we discuss the role of autophagy in the peripheral immune system and the CNS in neuroinfl ammation associated with the pathogenesis of MS. Keywords: autophagy; multiple sclerosis; neuro-infl ammation ·Review· IntroductionAutophagy, a lysosome-dependent degradation pathway, contributes to maintaining cellular homeostasis. Clearance of long-lived proteins, unnecessary organelles, and aggregate-prone proteins is mainly executed by autophagy for recycling cellular materials [1] . There are three subtypes of autophagy, macroautophagy, chaperone-mediated autophagy (CMA), and mitophagy. Macroautophagy is the major type for selective degradation of protein aggregates or misfolded proteins. The ubiquitin-labeled proteins are recognized by autophagy receptors, such as p62, neighbor of BRCA1 gene 1 (NBR1), and NIP3-like protein X (NIX), to form autophagosomes that then fuse with lysosomes for degradation. Many autophagy-related genes function during this process, such as Unc51-like kinase (ULK1) and autophagy-related gene (ATG) 5. Mammalian target of rapamycin (mTOR) represses autophagy by regulating ULK1 phosphorylation, while AMPK activates this process.CMA mediates the degradation of large molecular-weight proteins containing the KFERQ motif recognized by heat shock cognate protein of 70 kDa (HSC70). The substrate is then escorted to lysosome-associated membrane protein 2 (LAMP2A) for lysosomal degradation. Mitophagy is responsible for the degradation of damaged mitochondria.Parkin and PINK1 play critical roles in this process [2] . More Neurosci Bull August 1, 2015, 31(4): 435-444 436 attention has been paid to autophagy in the path...

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NOD2 stimulation induces autophagy in dendritic cells influencing bacterial handling and antigen presentation

Cited by 937 publications

References 25 publications

Intersection of autophagy with pathways of antigen presentation

Intersection of autophagy with pathways of antigen presentation

RIP kinases: key decision makers in cell death and innate immunity

Role of autophagy in the pathogenesis of multiple sclerosis

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