Role of Toll-like receptor signaling in the apoptotic response of macrophages to Yersinia infection
about
Cell death programs in Yersinia immunity and pathogenesisThe human-bacterial pathogen protein interaction networks of Bacillus anthracis, Francisella tularensis, and Yersinia pestisYersinia type III effectors perturb host innate immune responsesApplications of small molecule probes in dissecting mechanisms of bacterial virulence and host responsesIntegrating high-content imaging and chemical genetics to probe host cellular pathways critical for Yersinia pestis infectionMacrophage activation redirects yersinia-infected host cell death from apoptosis to caspase-1-dependent pyroptosis.Reduced secretion of YopJ by Yersinia limits in vivo cell death but enhances bacterial virulence.Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death.Caspase-8 mediates caspase-1 processing and innate immune defense in response to bacterial blockade of NF-κB and MAPK signalingA Yersinia effector with enhanced inhibitory activity on the NF-κB pathway activates the NLRP3/ASC/caspase-1 inflammasome in macrophagesYopJ-induced caspase-1 activation in Yersinia-infected macrophages: independent of apoptosis, linked to necrosis, dispensable for innate host defense.Yersinia pestis YopJ suppresses tumor necrosis factor alpha induction and contributes to apoptosis of immune cells in the lymph node but is not required for virulence in a rat model of bubonic plagueHemolysin induces Toll-like receptor (TLR)-independent apoptosis and multiple TLR-associated parallel activation of macrophages.Late repression of NF-κB activity by invasive but not non-invasive meningococcal isolates is required to display apoptosis of epithelial cells.Resistance to Yersinia pestis infection decreases with age in B10.T(6R) mice.Type III secretion system-dependent translocation of ectopically expressed Yop effectors into macrophages by intracellular Yersinia pseudotuberculosis.The expression and roles of Toll-like receptors in the biology of the human neutrophil.Activity of Uncleaved Caspase-8 Controls Anti-bacterial Immune Defense and TLR-Induced Cytokine Production Independent of Cell DeathNF-kappaB translocation prevents host cell death after low-dose challenge by Legionella pneumophila.Role of protein phosphorylation on serine/threonine and tyrosine in the virulence of bacterial pathogens.Yersinia virulence factor YopJ acts as a deubiquitinase to inhibit NF-kappa B activation.Type III secretion decreases bacterial and host survival following phagocytosis of Yersinia pseudotuberculosis by macrophages.Innate immune response during Yersinia infection: critical modulation of cell death mechanisms through phagocyte activation.Flagellin/TLR5 responses in epithelia reveal intertwined activation of inflammatory and apoptotic pathways.Modulation of innate immune responses by Yersinia type III secretion system translocators and effectors.Evasion and interference: intracellular pathogens modulate caspase-dependent inflammatory responses.Immunomodulatory Yersinia outer proteins (Yops)-useful tools for bacteria and humans alike.Cell-Extrinsic TNF Collaborates with TRIF Signaling To Promote Yersinia-Induced Apoptosis.Yersinia pestis and host macrophages: immunodeficiency of mouse macrophages induced by YscW.RIPK1-dependent apoptosis bypasses pathogen blockade of innate signaling to promote immune defense.YopJ targets TRAF proteins to inhibit TLR-mediated NF-kappaB, MAPK and IRF3 signal transduction.Increased expressions of ADAMTS-13 and apoptosis contribute to neuropathology during Toxoplasma gondii encephalitis in mice.Nucleotide-binding oligomerization domain 2 (Nod2) is dispensable for the innate immune responses of macrophages against Yersinia enterocolitica.Recombinant YopJ induces apoptosis in murine peritoneal macrophages in vitro: involvement of mitochondrial death pathway.Disparity between Yersinia pestis and Yersinia enterocolitica O:8 in YopJ/YopP-dependent functions.Absence of Toll-like receptor 4 signaling results in delayed Yersinia enterocolitica YopP-induced cell death of dendritic cells.Expression of the virulence factor, BfpA, by enteropathogenic Escherichia coli is essential for apoptosis signalling but not for NF-kappaB activation in host cells.Pattern Recognition Receptors and the Host Cell Death Molecular Machinery
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P2860
Role of Toll-like receptor signaling in the apoptotic response of macrophages to Yersinia infection
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2003 nî lūn-bûn
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2003 թուականի Մարտին հրատարակուած գիտական յօդուած
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2003 թվականի մարտին հրատարակված գիտական հոդված
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2003年の論文
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2003年論文
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2003年論文
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2003年論文
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2003年論文
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2003年論文
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2003年论文
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name
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@ast
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@en
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@nl
type
label
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@ast
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@en
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@nl
prefLabel
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@ast
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@en
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@nl
P2860
P921
P1476
Role of Toll-like receptor sig ...... rophages to Yersinia infection
@en
P2093
James B Bliska
P2860
P304
P356
10.1128/IAI.71.3.1513-1519.2003
P407
P577
2003-03-01T00:00:00Z