An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
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The emergence of Lyme diseaseBiology of infection with Borrelia burgdorferiBorrelia burgdorferi OspC protein required exclusively in a crucial early stage of mammalian infectionBorrelia burgdorferi changes its surface antigenic expression in response to host immune responsesOspC facilitates Borrelia burgdorferi invasion of Ixodes scapularis salivary glandsOuter-surface protein C of the Lyme disease spirochete: a protein induced in ticks for infection of mammalsTemporal expression analysis of the Borrelia burgdorferi paralogous gene family 54 genes BBA64, BBA65, and BBA66 during persistent infection in miceIncreasing the interaction of Borrelia burgdorferi with decorin significantly reduces the 50 percent infectious dose and severely impairs dissemination.Borrelia burgdorferi transcriptome in the central nervous system of non-human primates.Identification of Borrelia burgdorferi ribosomal protein L25 by the phage surface display method and evaluation of the protein's value for serodiagnosisPopulation-based study of diagnostic assays for Borrelia infection: comparison of purified flagella antigen assay (Ideia, Dako Cytomation) and recombinant antigen assay (Liaison, DiaSorin).bdrF2 of Lyme disease spirochetes is coexpressed with a series of cytoplasmic proteins and is produced specifically during early infection.Analysis of the dbpBA upstream regulatory region controlled by RpoS in Borrelia burgdorferi.Transcriptional responses of Leptospira interrogans to host innate immunity: significant changes in metabolism, oxygen tolerance, and outer membraneToll-like receptors 1 and 2 heterodimers alter Borrelia burgdorferi gene expression in mice and ticks.Outer surface protein C is a dissemination-facilitating factor of Borrelia burgdorferi during mammalian infection.Lipoprotein-dependent and -independent immune responses to spirochetal infection.Lymphoadenopathy during lyme borreliosis is caused by spirochete migration-induced specific B cell activationVariable tick protein in two genomic groups of the relapsing fever spirochete Borrelia hermsii in western North AmericaDynamics of connective-tissue localization during chronic Borrelia burgdorferi infectionBorrelia burgdorferi regulates expression of complement regulator-acquiring surface protein 1 during the mammal-tick infection cycle.Changes in temporal and spatial patterns of outer surface lipoprotein expression generate population heterogeneity and antigenic diversity in the Lyme disease spirochete, Borrelia burgdorferiOf ticks, mice and men: understanding the dual-host lifestyle of Lyme disease spirochaetes.Effect of Borrelia burgdorferi OspC at the site of inoculation in mouse skin.Evidence assessments and guideline recommendations in Lyme disease: the clinical management of known tick bites, erythema migrans rashes and persistent disease.Temporal analysis of the antigenic composition of Borrelia burgdorferi during infection in rabbit skin.Variable VlsE is critical for host reinfection by the Lyme disease spirochete.Delineating the requirement for the Borrelia burgdorferi virulence factor OspC in the mammalian host.Influence of arthritis-related protein (BBF01) on infectivity of Borrelia burgdorferi B31.In vivo expression technology identifies a novel virulence factor critical for Borrelia burgdorferi persistence in mice.Antigenic composition of Borrelia burgdorferi during infection of SCID mice.Comprehensive analysis of the factor h binding capabilities of borrelia species associated with lyme disease: delineation of two distinct classes of factor h binding proteinsProtective niche for Borrelia burgdorferi to evade humoral immunityA host-restricted viral vector for antigen-specific immunization against Lyme disease pathogen.The absence of linear plasmid 25 or 28-1 of Borrelia burgdorferi dramatically alters the kinetics of experimental infection via distinct mechanisms.Evaluation of the Importance of VlsE Antigenic Variation for the Enzootic Cycle of Borrelia burgdorferiRapid clearance of Lyme disease spirochetes lacking OspC from skin.Activation of the RpoN-RpoS regulatory pathway during the enzootic life cycle of Borrelia burgdorferi.Treatment of Lyme disease: a medicolegal assessment.Coordinated expression of Borrelia burgdorferi complement regulator-acquiring surface proteins during the Lyme disease spirochete's mammal-tick infection cycle.
P2860
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P2860
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年学术文章
@wuu
2002年学术文章
@zh-cn
2002年学术文章
@zh-hans
2002年学术文章
@zh-my
2002年学术文章
@zh-sg
2002年學術文章
@yue
2002年學術文章
@zh
2002年學術文章
@zh-hant
name
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
@ast
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
@en
type
label
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
@ast
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
@en
prefLabel
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
@ast
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
@en
P2093
P2860
P356
P1476
An immune evasion mechanism for spirochetal persistence in Lyme borreliosis.
@en
P2093
Fang Ting Liang
Lisa C Bowers
Mario T Philipp
Mary B Jacobs
P2860
P304
P356
10.1084/JEM.20011870
P407
P577
2002-02-01T00:00:00Z