Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
about
Mal connects TLR2 to PI3Kinase activation and phagocyte polarizationLipoproteins of Gram-Positive Bacteria: Key Players in the Immune Response and VirulenceInflammasome/IL-1β Responses to Streptococcal PathogensThe molecular mechanism of bacterial lipoprotein modification--how, when and why?Recent advances in understanding the molecular basis of group B Streptococcus virulenceEnterococcus faecalis Glycolipids Modulate Lipoprotein-Content of the Bacterial Cell Membrane and Host Immune ResponseTLR2 mediates recognition of live Staphylococcus epidermidis and clearance of bacteremiaToll-like receptor 1 polymorphisms affect innate immune responses and outcomes in sepsis.Prospective virtual screening in a sparse data scenario: design of small-molecule TLR2 antagonists.Induction and termination of inflammatory signaling in group B streptococcal sepsis.Type I interferon production induced by Streptococcus pyogenes-derived nucleic acids is required for host protectionLgt processing is an essential step in Streptococcus suis lipoprotein mediated innate immune activation.Lipoproteins of bacterial pathogens.Essential role of interleukin-1 signaling in host defenses against group B streptococcus.TLR-mediated inflammatory responses to Streptococcus pneumoniae are highly dependent on surface expression of bacterial lipoproteinsComplete genome sequence of the frog pathogen Mycobacterium ulcerans ecovar LiflandiiEffects of deletion of the Streptococcus pneumoniae lipoprotein diacylglyceryl transferase gene lgt on ABC transporter function and on growth in vivo.Interaction of Streptococcus agalactiae and Cellular Innate Immunity in Colonization and DiseaseMacrophages recognize streptococci through bacterial single-stranded RNAThe interleukin-1β/CXCL1/2/neutrophil axis mediates host protection against group B streptococcal infection.Morphine inhibits murine dendritic cell IL-23 production by modulating Toll-like receptor 2 and Nod2 signaling.Toll-like receptor 2-independent host innate immune response against an epidemic strain of Streptococcus suis that causes a toxic shock-like syndrome in humansNeonatal immune adaptation of the gut and its role during infections.Immune activation and suppression by group B streptococcus in a murine model of urinary tract infectionLipoprotein biosynthesis by prolipoprotein diacylglyceryl transferase is required for efficient spore germination and full virulence of Bacillus anthracis.NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNASurface-Associated Lipoproteins Link Enterococcus faecalis Virulence to Colitogenic Activity in IL-10-Deficient Mice Independent of Their Expression LevelsActivation of the NLRP3 inflammasome by group B streptococciNovel bacterial lipoprotein structures conserved in low-GC content gram-positive bacteria are recognized by Toll-like receptor 2.The Human Pathogen Streptococcus pyogenes Releases Lipoproteins as Lipoprotein-rich Membrane VesiclesNeutrophils Directly Recognize Group B Streptococci and Contribute to Interleukin-1β Production during Infection.Single nucleotide polymorphisms in toll-like receptor 6 are associated with altered lipopeptide- and mycobacteria-induced interleukin-6 secretionHumanized mice, a new model to study the influence of drug treatment on neonatal sepsisGroup B Streptococcus induces a caspase-dependent apoptosis in fetal rat lung interstitium.The Triacylated ATP Binding Cluster Transporter Substrate-binding Lipoprotein of Staphylococcus aureus Functions as a Native Ligand for Toll-like Receptor 2Toll-like receptor 2 deficiency is associated with enhanced severity of group B streptococcal disease.Contribution of lipoproteins and lipoprotein processing to endocarditis virulence in Streptococcus sanguinisLipoprotein lipase and hydrofluoric acid deactivate both bacterial lipoproteins and lipoteichoic acids, but platelet-activating factor-acetylhydrolase degrades only lipoteichoic acidsExtracellular nucleotide catabolism by the Group B Streptococcus ectonucleotidase NudP increases bacterial survival in blood.A phylum level analysis reveals lipoprotein biosynthesis to be a fundamental property of bacteria.
P2860
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P2860
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh-hant
name
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
@en
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
@nl
type
label
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
@en
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
@nl
prefLabel
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
@en
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis.
@nl
P2093
P50
P921
P1476
Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis
@en
P2093
Douglas T Golenbock
Elisabeth Pellegrini
Giuseppe Mancuso
Giuseppe Teti
Johannes Hübner
Kamila Chraibi
Philipp Henneke
Sandra Santos-Sierra
Shaynoor Dramsi
P304
P356
10.4049/JIMMUNOL.180.9.6149
P407
P577
2008-05-01T00:00:00Z