T cell-activation in neuromyelitis optica lesions plays a role in their formation.
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Antibodies as Mediators of Brain PathologyTreatment of neuromyelitis optica: state-of-the-art and emerging therapiesAdvances in Autoimmune Epilepsy Associated with Antibodies, Their Potential Pathogenic Molecular Mechanisms, and Current Recommended ImmunotherapiesEfficacy and safety of tacrolimus treatment for neuromyelitis optica spectrum disorderExpanding Role of T Cells in Human Autoimmune Diseases of the Central Nervous System.Systemic inflammation and the brain: novel roles of genetic, molecular, and environmental cues as drivers of neurodegeneration.Neuromyelitis optica pathology in rats following intraperitoneal injection of NMO-IgG and intracerebral needle injury.Markedly increased IP-10 production by blood-brain barrier in neuromyelitis opticaExperimental Neuromyelitis Optica Induces a Type I Interferon Signature in the Spinal Cord.Highly encephalitogenic aquaporin 4-specific T cells and NMO-IgG jointly orchestrate lesion location and tissue damage in the CNS.Severely exacerbated neuromyelitis optica rat model with extensive astrocytopathy by high affinity anti-aquaporin-4 monoclonal antibody.Aquaporin 4-specific T cells and NMO-IgG cause primary retinal damage in experimental NMO/SDMultiple sclerosis: experimental models and reality.Astrocyte barriers to neurotoxic inflammation.Neuromyelitis optica: a positive appraisal of seronegative cases.OX40, OX40L and Autoimmunity: a Comprehensive Review.Neurodegeneration in multiple sclerosis and neuromyelitis optica.Müller cells and retinal axons can be primary targets in experimental neuromyelitis optica spectrum disorder.The Role of Brain-Reactive Autoantibodies in Brain Pathology and Cognitive Impairment.Neuromyelitis optica study model based on chronic infusion of autoantibodies in rat cerebrospinal fluid.IgG and complement deposition and neuronal loss in cats and humans with epilepsy and voltage-gated potassium channel complex antibodies.Human antibodies against the myelin oligodendrocyte glycoprotein can cause complement-dependent demyelination.Association of TNFSF4 Polymorphisms with Neuromyelitis Optica Spectrum Disorders in a Chinese Population.Impact of Autologous Mesenchymal Stem Cell Infusion on Neuromyelitis Optica Spectrum Disorder: A Pilot, 2-Year Observational Study.Mechanisms for lesion localization in neuromyelitis optica spectrum disorders.Early and extensive spinal white matter involvement in neuromyelitis optica.OX40 Gene and Serum Protein Expression Profiles in Patients with Parkinson's Disease.Prediction of disease severity in neuromyelitis optica by the levels of interleukin (IL)-6 produced during remission phase.The compartmentalized inflammatory response in the multiple sclerosis brain is composed of tissue-resident CD8+ T lymphocytes and B cells.
P2860
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P2860
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
@en
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
@nl
type
label
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
@en
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
@nl
prefLabel
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
@en
T cell-activation in neuromyelitis optica lesions plays a role in their formation.
@nl
P2093
P2860
P50
P356
P1476
T cell-activation in neuromyelitis optica lesions plays a role in their formation
@en
P2093
Hartmut Wekerle
Joachim W Ellwart
Joana Machado-Santos
Kazuo Fujihara
Maja Kitic
Maria Pohl
Marie-Therese Fischer
Naoto Kawakami
Tatsuro Misu
P2860
P2888
P356
10.1186/2051-5960-1-85
P577
2013-12-24T00:00:00Z
P5875
P6179
1017867931