about
Hypersensitivity Responses in the Central Nervous SystemReactive microgliosis engages distinct responses by microglial subpopulations after minor central nervous system injuryAxotomy-induced glial reactions in normal and cytokine transgenic mice.Influence of type I IFN signaling on anti-MOG antibody-mediated demyelination.Chemokine receptor expression by inflammatory T cells in EAE.Immune regulation and CNS autoimmune disease.Surfactant protein d deficiency in mice is associated with hyperphagia, altered fat deposition, insulin resistance, and increased basal endotoxemia.TNFalpha: kill or cure for demyelinating disease?Chemokines in experimental autoimmune encephalomyelitis and multiple sclerosis.Continued administration of ciliary neurotrophic factor protects mice from inflammatory pathology in experimental autoimmune encephalomyelitis.Stimulation of adult oligodendrogenesis by myelin-specific T cellsInterferon regulatory factor-7 modulates experimental autoimmune encephalomyelitis in mice.Induction of endogenous Type I interferon within the central nervous system plays a protective role in experimental autoimmune encephalomyelitis.TLR3 deficiency renders astrocytes permissive to herpes simplex virus infection and facilitates establishment of CNS infection in miceCerebrospinal fluid aquaporin-4-immunoglobulin G disrupts blood brain barrier.Pathologic and Protective Roles for Microglial Subsets and Bone Marrow- and Blood-Derived Myeloid Cells in Central Nervous System Inflammation.The changing face of cytokines in the brain: perspectives from EAE.Blood-brain barrier disruption in CCL2 transgenic mice during pertussis toxin-induced brain inflammation.Animal models for multiple sclerosis.T-dependent B-cell activation is signalled by an early increase in potassium influx.CD8+ T cells in inflammatory demyelinating disease.Statin therapy inhibits remyelination in the central nervous system.Toll-like receptors in neurodegeneration.Comparison of microglia and infiltrating CD11c⁺ cells as antigen presenting cells for T cell proliferation and cytokine response.Neuromyelitis optica (NMO)--an autoimmune disease of the central nervous system (CNS).Innate immune responses in central nervous system inflammation.Interferons in the central nervous system: a few instruments play many tunes.What is microglia neurotoxicity (Not)?The cell biology of T-dependent B cell activation.Inflammation in the central nervous system and Th17 responses are inhibited by IFN-gamma-Induced IL-18 binding protein.The murine gammaherpesvirus-68 chemokine-binding protein M3 inhibits experimental autoimmune encephalomyelitis.Vav-1 expression correlates with NFκB activation and CD40-mediated cell death in diffuse large B-cell lymphoma cell lines.Constitutive activation of extracellular signal-regulated kinase predisposes diffuse large B-cell lymphoma cell lines to CD40-mediated cell death.T-cell costimulation: T cells themselves call the shots.Effectors of Th1 and Th17 cells act on astrocytes and augment their neuroinflammatory properties.Detection and cellular localization of phospho-STAT2 in the central nervous system by immunohistochemical staining.IFN-gamma-induced chemokines synergize with pertussis toxin to promote T cell entry to the central nervous system.Helper T cell lines to major and to minor histocompatibility antigens are equally effective in the regulation of B cell responses in vivo.Bone marrow-derived versus parenchymal sources of inducible nitric oxide synthase in experimental autoimmune encephalomyelitis.Microglia are required for astroglial Toll-like receptor 4 response and for optimal TLR2 and TLR3 response.
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description
hulumtues
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researcher
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հետազոտող
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name
Trevor Owens
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Trevor Owens
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Trevor Owens
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Trevor Owens
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Trevor Owens
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تريفور أوينز
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Trevor Owens
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Trevor Owens
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Trevor Owens
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Trevor Owens
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Trevor Owens
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تريفور أوينز
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Trevor Owens
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Trevor Owens
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Trevor Owens
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Trevor Owens
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Trevor Owens
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تريفور أوينز
@ar
P106
P1153
7101750869
P21
P2798
P31
P496
0000-0001-9315-6036