Acute experimental autoimmune encephalomyelitis in mice. I. Adjuvant action of Bordetella pertussis is due to vasoactive amine sensitization and increased vascular permeability of the central nervous system.
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The PD-1 pathway in tolerance and autoimmunityFocal transient CNS vessel leak provides a tissue niche for sequential immune cell accumulation during the asymptomatic phase of EAE induction.Pertussis toxin transiently affects barrier integrity, organelle organization and transmigration of monocytes in a human brain microvascular endothelial cell barrier modelAbsence of monocyte chemoattractant protein 1 in mice leads to decreased local macrophage recruitment and antigen-specific T helper cell type 1 immune response in experimental autoimmune encephalomyelitisRole of pertussis toxin A subunit in neutrophil migration and vascular permeability.An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.Paradoxical effect of pertussis toxin on the delayed hypersensitivity response to autoantigens in mice.Tolerance and autoimmunity in TCR transgenic mice specific for myelin basic protein.Anaphylaxis and mortality induced by treatment of mice with anti-VLA-4 antibody and pertussis toxin.Pertussis toxin up-regulates angiotensin type 1 receptors through Toll-like receptor 4-mediated Rac activation.Peripheral and central neuronal ATF3 precedes CD4+ T-cell infiltration in EAE.Endothelial histamine H1 receptor signaling reduces blood-brain barrier permeability and susceptibility to autoimmune encephalomyelitis.Active induction of experimental autoimmune encephalomyelitis by MOG35-55 peptide immunization is associated with differential responses in separate compartments of the choroid plexusIL-11 regulates autoimmune demyelinationG(i/o) protein-dependent and -independent actions of Pertussis Toxin (PTX).Osteopontin expression in the brain triggers localized inflammation and cell death when immune cells are activated by pertussis toxin.Analysis of the role of Bphs/Hrh1 in the genetic control of responsiveness to pertussis toxin.Multiple elements of the allergic arm of the immune response modulate autoimmune demyelination.In vivo anti-LAP mAb enhances IL-17/IFN-γ responses and abrogates anti-CD3-induced oral tolerance.Attenuation of Th1 effector cell responses and susceptibility to experimental allergic encephalomyelitis in histamine H2 receptor knockout mice is due to dysregulation of cytokine production by antigen-presenting cells.Antibiotic treatment attenuates behavioral and neurochemical changes induced by exposure of rats to group a streptococcal antigenBrain-reactive antibodies and disease.Encephalitogenic potential of myelin basic protein-specific T cells isolated from normal rhesus macaquesMechanisms of edema formation in experimental autoimmune encephalomyelitis. The contribution of inflammatory cells.Central histamine H3 receptor signaling negatively regulates susceptibility to autoimmune inflammatory disease of the CNS.Glia-dependent TGF-beta signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis.Meningeal Infiltration of the Spinal Cord by Non-Classically Activated B Cells is Associated with Chronic Disease Course in a Spontaneous B Cell-Dependent Model of CNS Autoimmune DiseaseBehavioral, pharmacological, and immunological abnormalities after streptococcal exposure: a novel rat model of Sydenham chorea and related neuropsychiatric disorders.Blood-brain barrier disruption in CCL2 transgenic mice during pertussis toxin-induced brain inflammation.Pertussis Toxin Is a Robust and Selective Inhibitor of High Grade Glioma Cell Migration and Invasion.Locus controlling Bordetella pertussis-induced histamine sensitization (Bphs), an autoimmune disease-susceptibility gene, maps distal to T-cell receptor beta-chain gene on mouse chromosome 6.Transfer of experimental allergic encephalomyelitis to bone marrow chimeras. Endothelial cells are not a restricting elementExperimental priming of encephalitogenic Th1/Th17 cells requires pertussis toxin-driven IL-1β production by myeloid cellsRole of toll-like receptors in multiple sclerosis.Effect of pertussigen on inflammation caused by Freund adjuvantNeurovascular damage in experimental allergic encephalomyelitis: a target for pharmacological control.Activation of antigen-presenting cells by microbial products breaks self tolerance and induces autoimmune disease.Pertussis toxin-induced cytokine differentiation and clonal expansion of T cells is mediated predominantly via costimulation.B7-H1 shapes T-cell-mediated brain endothelial cell dysfunction and regional encephalitogenicity in spontaneous CNS autoimmunity.Murine autoimmune hearing loss mediated by CD4+ T cells specific for inner ear peptides.
P2860
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P2860
Acute experimental autoimmune encephalomyelitis in mice. I. Adjuvant action of Bordetella pertussis is due to vasoactive amine sensitization and increased vascular permeability of the central nervous system.
description
1982 nî lūn-bûn
@nan
1982年の論文
@ja
1982年学术文章
@wuu
1982年学术文章
@zh-cn
1982年学术文章
@zh-hans
1982年学术文章
@zh-my
1982年学术文章
@zh-sg
1982年學術文章
@yue
1982年學術文章
@zh
1982年學術文章
@zh-hant
name
Acute experimental autoimmune ...... of the central nervous system.
@en
Acute experimental autoimmune ...... of the central nervous system.
@nl
type
label
Acute experimental autoimmune ...... of the central nervous system.
@en
Acute experimental autoimmune ...... of the central nervous system.
@nl
prefLabel
Acute experimental autoimmune ...... of the central nervous system.
@en
Acute experimental autoimmune ...... of the central nervous system.
@nl
P2093
P1433
P1476
Acute experimental autoimmune ...... of the central nervous system.
@en
P2093
A Blaskett
D S Linthicum
P304
P356
10.1016/0008-8749(82)90457-9
P577
1982-11-01T00:00:00Z