About: TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection

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About: TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection Goto Sponge NotDistinct Permalink

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scientific article published on 30 December 2009

Attributes	Values
rdf:type	Item
description	wetenschappelijk artikel (nl) article scientifique publié en 2009 (fr) наукова стаття, опублікована в грудні 2009 (uk) im Dezember 2009 veröffentlichter wissenschaftlicher Artikel (de) scientific article published on 30 December 2009 (en) artículu científicu espublizáu n'avientu de 2009 (ast)
publication date	wds:Q82370199-02F7EF67-C30C-440A-972C-1F0A45F5981C
publication date	2009-12-30 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q82370199-52FE8FCF-9DE3-4237-AFE1-0D2AFD9A063C
language of work or name	English
cites work	wds:Q82370199-79FCA278-9EA5-480B-8317-89A7A2AF815D
cites work	Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene
author name string	wds:Q82370199-6714D9A7-7C7D-4344-8F86-A5904308F479 wds:Q82370199-79701529-10DA-4342-82EE-6C6E36E6F488 wds:Q82370199-8DA5ECDF-D00B-48D7-8B1F-E0FF8A777679
author name string	Shizuo Akira Elia Burns Tal Eliyahu
rdfs:label	TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection (en) TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection (nl)
skos:prefLabel	TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection (en) TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection (nl)
name	TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection (en) TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection (nl)
author	wds:Q82370199-5641362B-45AF-4780-A043-E7562D7DBEDC wds:Q82370199-B4A32D49-BD56-4552-8C4C-8DA6DFC6B206
author	Gabriel Nussbaum Satoshi Uematsu
title	wds:Q82370199-33A8FEE5-15DD-4802-999E-F89FD47DCC03
title	TLR2-dependent inflammatory response to Porphyromonas gingivalis is MyD88 independent, whereas MyD88 is required to clear infection (en)
page(s)	wds:Q82370199-E62897D9-B0E9-41B0-A7FF-B6ED885D4839
page(s)	1455-1462
instance of	wds:Q82370199-BE4800B2-38D8-4D55-AFCF-BA39CE01B3DC
instance of	scholarly article
main subject	wds:Q82370199-765B32D0-A28C-4F2B-AEFB-7B33182B6976
main subject	Porphyromonas gingivalis
PubMed ID	wds:Q82370199-6F635DBD-142B-471F-ADCE-5FAA09374610
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/20042569
PubMed ID	20042569
published in	wds:Q82370199-DD54ABFC-3ACE-4629-B950-92235CBAAC0E
published in	Journal of Immunology
issue	wds:Q82370199-2E18E6F4-3C0A-4C4E-9D81-3071C4D5D58B
volume	wds:Q82370199-AD060EAD-E2D2-4071-AB8E-8FCA025191F8
issue	3
volume	184
DOI	wds:Q82370199-00A6BA5E-D9BB-4CDF-A8AB-FB6246F7566E
DOI	http://dx.doi.org/10.4049/JIMMUNOL.0900378
DOI	10.4049/JIMMUNOL.0900378
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q82370199
is cites work of	Neutrophil homeostasis and inflammation: novel paradigms from studying periodontitis Porphyromonas gingivalis manipulates complement and TLR signaling to uncouple bacterial clearance from inflammation and promote dysbiosis Review: Pathogen-induced inflammation at sites distant from oral infection: bacterial persistence and induction of cell-specific innate immune inflammatory pathways. Sphingosine kinase-1 is required for toll mediated beta-defensin 2 induction in human oral keratinocytes Tetra- and penta-acylated lipid A structures of Porphyromonas gingivalis LPS differentially activate TLR4-mediated NF-κB signal transduction cascade and immuno-inflammatory response in human gingival fibroblasts Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3 TLR2, TLR4 and CD14 recognize venom-associated molecular patterns from Tityus serrulatus to induce macrophage-derived inflammatory mediators Pathogenic bacterial species associated with endodontic infection evade innate immune control by disabling neutrophils Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis Role of MyD88-dependent and MyD88-independent signaling in Porphyromonas gingivalis-elicited macrophage foam cell formation. TLR-Dependent Human Mucosal Epithelial Cell Responses to Microbial Pathogens More than complementing Tolls: complement-Toll-like receptor synergy and crosstalk in innate immunity and inflammation Immune and regulatory functions of neutrophils in inflammatory bone loss Immuno-pathogenesis of Periodontal Disease: Current and Emerging Paradigms CD36/SR-B2-TLR2 Dependent Pathways Enhance Porphyromonas gingivalis Mediated Atherosclerosis in the Ldlr KO Mouse Model mRNA expression of pattern recognition receptors and their signaling mediators in healthy and diseased gingival tissues. The oral microbiota: dynamic communities and host interactions Mobilization of endothelial progenitors by recurrent bacteremias with a periodontal pathogen Porphyromonas gingivalis promotes neointimal formation after arterial injury through toll-like receptor 2 signaling Major neutrophil functions subverted by Porphyromonas gingivalis Interferon regulatory factor 6 differentially regulates Toll-like receptor 2-dependent chemokine gene expression in epithelial cells. TLR2-dependent pathway of heterologous down-modulation for the CC chemokine receptors 1, 2, and 5 in human blood monocytes Multiple roles of Myd88 in the immune response to the plague F1-V vaccine and in protection against an aerosol challenge of Yersinia pestis CO92 in mice Liver X receptors contribute to periodontal pathogen-elicited inflammation and oral bone loss Neutrophil Functions in Periodontal Homeostasis Immunologic environment influences macrophage response to Porphyromonas gingivalis. Porphyromonas gingivalis Stimulates TLR2-PI3K Signaling to Escape Immune Clearance and Induce Bone Resorption Independently of MyD88. The Pros1/Tyro3 axis protects against periodontitis by modulating STAT/SOCS signalling Periodontitis and myocardial hypertrophy Pathogenesis of Important Virulence Factors of Porphyromonas gingivalis via Toll-Like Receptors Linkage of Infection to Adverse Systemic Complications: Periodontal Disease, Toll-Like Receptors, and Other Pattern Recognition Systems. Intragingival injection of Porphyromonas gingivalis-derived lipopolysaccharide induces a transient increase in gingival tumour necrosis factor-α, but not interleukin-6, in anaesthetised rats Toll Like Receptors Signaling Pathways as a Target for Therapeutic Interventions The Distinct Immune-Stimulatory Capacities of Porphyromonas gingivalis Strains 381 and ATCC 33277 Are Determined by the fimB Allele and Gingipain Activity
is cites work of	wds:Q28080991-4D43211F-12E3-401F-AF44-D85A4414EE91 wds:Q33634084-07F69828-94A4-4E5B-99D5-CE0AF418A841 wds:Q33807749-D67E551B-C39D-4D4C-B2A3-8EEC3925408A wds:Q38991040-4A55AFC0-CEE9-4EC6-BB92-C57A9E9D7AFC wds:Q24315160-DB71A6FC-1B12-4AEE-A5C0-572ED8AEE5C7 wds:Q33786763-AC1E0BF4-0209-4437-8CD0-0E6F1115CCE1 wds:Q36258207-42D183CD-033B-4D5B-91A0-0DD950E01BD7 wds:Q64279701-C73A7004-76E5-4F1C-8C60-8CBB6510FEBB wds:Q35566496-97D333BF-2A70-4119-BD95-BE3B61A049F9 wds:Q36704913-BEA112F3-1F7C-44E1-95DF-D13576B8E5D4 wds:Q39004036-AFD8A893-97AD-4093-8DBA-E3389FBB7BEE wds:Q44255321-CE424E78-2FE1-46B4-9AD5-F48A0EE16DD9 wds:Q42003231-1B192B27-B996-4936-A2F2-54504DD8124F wds:Q36091804-BC139886-203B-4F1A-A7DB-21A1BC68C7DA wds:Q34181823-69924442-5958-45DA-8F81-FD7D4A0DA8AC wds:Q41331276-E9B74ECF-77EC-4C7D-94C7-BE299A27DDD4

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