Mice lacking components of adaptive immunity show increased Brucella abortus virB mutant colonization.
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Establishment of Chronic Infection: Brucella's Stealth StrategyType IV secretion system of Brucella spp. and its effectorsRNAi screen of endoplasmic reticulum-associated host factors reveals a role for IRE1alpha in supporting Brucella replication.Innate immune recognition of flagellin limits systemic persistence of BrucellaIn situ microscopy analysis reveals local innate immune response developed around Brucella infected cells in resistant and susceptible mice.The Vi capsular polysaccharide prevents complement receptor 3-mediated clearance of Salmonella enterica serotype Typhi.Laboratory animal models for brucellosis research.The predicted ABC transporter AbcEDCBA is required for type IV secretion system expression and lysosomal evasion by Brucella ovis.CD4+ T cell-derived IL-10 promotes Brucella abortus persistence via modulation of macrophage function.Establishment of systemic Brucella melitensis infection through the digestive tract requires urease, the type IV secretion system, and lipopolysaccharide O antigenWhat have we learned from brucellosis in the mouse model?Crucial role of gamma interferon-producing CD4+ Th1 cells but dispensable function of CD8+ T cell, B cell, Th2, and Th17 responses in the control of Brucella melitensis infection in mice.VirB12 is a serological marker of Brucella infection in experimental and natural hosts.Inactivation of the type IV secretion system reduces the Th1 polarization of the immune response to Brucella abortus infection.VirB3 to VirB6 and VirB8 to VirB11, but not VirB7, are essential for mediating persistence of Brucella in the reticuloendothelial system.Sensing of bacterial type IV secretion via the unfolded protein response.NOD1 and NOD2 signalling links ER stress with inflammation.PPARγ-mediated increase in glucose availability sustains chronic Brucella abortus infection in alternatively activated macrophages.Contribution of flagellin pattern recognition to intestinal inflammation during Salmonella enterica serotype typhimurium infectionNatural antibody contributes to host defense against an attenuated Brucella abortus virB mutant.Responses to amyloids of microbial and host origin are mediated through toll-like receptor 2.An evolutionary strategy for a stealthy intracellular Brucella pathogen.Brucellosis and type IV secretion.Internal affairs: investigating the Brucella intracellular lifestyle.Brucella evasion of adaptive immunity.Chronic Bacterial Pathogens: Mechanisms of Persistence.The Vi-capsule prevents Toll-like receptor 4 recognition of Salmonella.Systems Biology Analysis of Temporal In vivo Brucella melitensis and Bovine Transcriptomes Predicts host:Pathogen Protein-Protein Interactions.Utilization of host polyamines in alternatively activated macrophages promotes chronic infection by Brucella abortus.
P2860
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P2860
Mice lacking components of adaptive immunity show increased Brucella abortus virB mutant colonization.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Mice lacking components of ada ...... rtus virB mutant colonization.
@en
type
label
Mice lacking components of ada ...... rtus virB mutant colonization.
@en
prefLabel
Mice lacking components of ada ...... rtus virB mutant colonization.
@en
P2860
P356
P1476
Mice lacking components of ada ...... rtus virB mutant colonization.
@en
P2093
Hortensia García Rolán
P2860
P304
P356
10.1128/IAI.01896-06
P407
P577
2007-04-09T00:00:00Z