The Lyme disease spirochete Borrelia burgdorferi utilizes multiple ligands, including RNA, for interferon regulatory factor 3-dependent induction of type I interferon-responsive genes
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Mechanisms of Borrelia burgdorferi internalization and intracellular innate immune signalingPhagosomal signaling by Borrelia burgdorferi in human monocytes involves Toll-like receptor (TLR) 2 and TLR8 cooperativity and TLR8-mediated induction of IFN-betaBorrelia burgdorferi RNA induces type I and III interferons via Toll-like receptor 7 and contributes to production of NF-κB-dependent cytokinesNod2 suppresses Borrelia burgdorferi mediated murine Lyme arthritis and carditis through the induction of tolerance.Different patterns of expression and of IL-10 modulation of inflammatory mediators from macrophages of Lyme disease-resistant and -susceptible mice.Innate immunity networks during infection with Borrelia burgdorferi.Borrelia burgdorferi arthritis-associated locus Bbaa1 regulates Lyme arthritis and K/B×N serum transfer arthritis through intrinsic control of type I IFN production.Induction of indoleamine 2,3-dioxygenase by Borrelia burgdorferi in human immune cells correlates with pathogenic potential.Intracellular Concentrations of Borrelia burgdorferi Cyclic Di-AMP Are Not Changed by Altered Expression of the CdaA SynthaseBorrelia burgdorferi induces a type I interferon response during early stages of disseminated infection in mice.Homogeneous Inflammatory Gene Profiles Induced in Human Dermal Fibroblasts in Response to the Three Main Species of Borrelia burgdorferi sensu lato.MyD88- and TRIF-independent induction of type I interferon drives naive B cell accumulation but not loss of lymph node architecture in Lyme disease.TRIF mediates Toll-like receptor 2-dependent inflammatory responses to Borrelia burgdorferi.Endothelial cells and fibroblasts amplify the arthritogenic type I IFN response in murine Lyme disease and are major sources of chemokines in Borrelia burgdorferi-infected joint tissue.Tick saliva suppresses IFN signalling in dendritic cells upon Borrelia afzelii infection.Borrelia burgdorferi BbHtrA degrades host ECM proteins and stimulates release of inflammatory cytokines in vitro.Genetic Control of Lyme Arthritis by Borrelia burgdorferi Arthritis-Associated Locus 1 Is Dependent on Localized Differential Production of IFN-β and Requires Upregulation of Myostatin.
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P2860
The Lyme disease spirochete Borrelia burgdorferi utilizes multiple ligands, including RNA, for interferon regulatory factor 3-dependent induction of type I interferon-responsive genes
description
2010 nî lūn-bûn
@nan
2010年の論文
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2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
2010年论文
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2010年论文
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name
The Lyme disease spirochete Bo ...... I interferon-responsive genes
@en
type
label
The Lyme disease spirochete Bo ...... I interferon-responsive genes
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prefLabel
The Lyme disease spirochete Bo ...... I interferon-responsive genes
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P2093
P2860
P356
P1476
The Lyme disease spirochete Bo ...... I interferon-responsive genes
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P2093
Heather Maylor-Hagen
Janis J Weis
Jennifer C Miller
John H Weis
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P304
P356
10.1128/IAI.01070-09
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P577
2010-04-19T00:00:00Z