Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
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Relative contributions of innate and acquired host responses to bacterial control and arthritis development in Lyme diseaseInterleukin-4 (IL-4) and IL-13 signaling pathways do not regulate Borrelia burgdorferi-induced arthritis in mice: IgG1 is not required for host control of tissue spirochetes.Lyme borreliosis in rhesus macaques: effects of corticosteroids on spirochetal load and isotype switching of anti-borrelia burgdorferi antibody.Early induction of gamma interferon and interleukin-10 production in draining lymph nodes from mice infected with Borrelia burgdorferi.Activation of endothelium by Borrelia burgdorferi in vitro enhances transmigration of specific subsets of T lymphocytesCoinfection with Borrelia burgdorferi and the agent of human granulocytic ehrlichiosis alters murine immune responses, pathogen burden, and severity of Lyme arthritis.Gamma interferon is not required for arthritis resistance in the murine Lyme disease modelCD4+ T helper 1 cells facilitate regression of murine Lyme carditisInvariant NKT cell development requires a full complement of functional CD3 zeta immunoreceptor tyrosine-based activation motifsDifferent patterns of expression and of IL-10 modulation of inflammatory mediators from macrophages of Lyme disease-resistant and -susceptible mice.OspE-related, OspF-related, and Elp lipoproteins are immunogenic in baboons experimentally infected with Borrelia burgdorferi and in human lyme disease patients.A critical role for type I IFN in arthritis development following Borrelia burgdorferi infection of mice.CD4+ T cells promote antibody production but not sustained affinity maturation during Borrelia burgdorferi infection.Inhibition of interleukin-17 prevents the development of arthritis in vaccinated mice challenged with Borrelia burgdorferi.Murine Lyme arthritis development mediated by p38 mitogen-activated protein kinase activity.Control of Borrelia burgdorferi-specific CD4+-T-cell effector function by interleukin-12- and T-cell receptor-induced p38 mitogen-activated protein kinase activityPhagocytosis of Borrelia burgdorferi and Treponema pallidum potentiates innate immune activation and induces gamma interferon productionGene expression profiling provides insights into the pathways involved in inflammatory arthritis development: murine model of Lyme disease.Lyme arthritis: current concepts and a change in paradigm.NKT cells prevent chronic joint inflammation after infection with Borrelia burgdorferi.Local production of IFN-gamma by invariant NKT cells modulates acute Lyme carditisDiagnostic value of cytokines and chemokines in lyme neuroborreliosis.Association of CD4+ CD25+ T cells with prevention of severe destructive arthritis in Borrelia burgdorferi-vaccinated and challenged gamma interferon-deficient mice treated with anti-interleukin-17 antibody.Borrelia species induce inflammasome activation and IL-17 production through a caspase-1-dependent mechanismHamster and murine models of severe destructive Lyme arthritis.The potential for genetically altered microglia to influence glioma treatment.Interferon-γ influences the composition of leukocytic infiltrates in murine lyme carditis.Destructive arthritis in vaccinated interferon gamma-deficient mice challenged with Borrelia burgdorferi: modulation by tumor necrosis factor alpha.Humoral immunity reflects altered T helper cell bias in Borrelia burgdorferi-infected gamma delta T-cell-deficient mice.Neutralization of gamma interferon augments borreliacidal antibody production and severe destructive Lyme arthritis in C3H/HeJ mice.Localized production of IL-10 suppresses early inflammatory cell infiltration and subsequent development of IFN-γ-mediated Lyme arthritisInterleukin-35 enhances Lyme arthritis in Borrelia-vaccinated and -infected mice.Interleukin-23 is required for development of arthritis in mice vaccinated and challenged with Borrelia species.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.Interleukin-10 (IL-10) inhibits Borrelia burgdorferi-induced IL-17 production and attenuates IL-17-mediated Lyme arthritis.IL-10 Deficiency Reveals a Role for TLR2-Dependent Bystander Activation of T Cells in Lyme Arthritis.Mercury exposure as a model for deviation of cytokine responses in experimental Lyme arthritis: HgCl2 treatment decreases T helper cell type 1-like responses and arthritis severity but delays eradication of Borrelia burgdorferi in C3H/HeN mice.
P2860
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P2860
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
description
1999 nî lūn-bûn
@nan
1999 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
@ast
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
@en
type
label
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
@ast
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
@en
prefLabel
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
@ast
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
@en
P2860
P1476
Experimental lyme arthritis in the absence of interleukin-4 or gamma interferon.
@en
P2093
P2860
P304
P407
P577
1999-07-01T00:00:00Z