نتایج جستجو برای: experimental autoimmune encephalomyelitis eae
تعداد نتایج: 767110 فیلتر نتایج به سال:
We explore here if vaccination with DNA encoding an autoantigenic peptide can suppress autoimmune disease. For this purpose we used experimental autoimmune encephalomyelitis (EAE), which is an autoaggressive disease in the central nervous system and an animal model for multiple sclerosis. Lewis rats were vaccinated with DNA encoding an encephalitogenic T cell epitope, guinea pig myelin basic pr...
The adoptive transfer of myelin-reactive T cells into wild-type hosts results in spinal cord inflammation and ascending paralysis, referred to as conventional experimental autoimmune encephalomyelitis (EAE), as opposed to brainstem inflammation and ataxia, which characterize disease in IFN-γRKO hosts (atypical EAE). In this article, we show that atypical EAE correlates with preferential upregul...
Thank you for the submission of your manuscript "Inhibition of the immunoproteasome strongly ameliorates experimental autoimmune encephalomyelitis (EAE)". We have now heard back from the three referees whom we asked to evaluate your manuscript. As you will see, the referees acknowledge that the overall topic of the manuscript is potentially interesting. However, they also raise significant conc...
Multiple sclerosis (MS) is a chronic autoimmune disease that affects the myelination of neurons present in central nervous system (CNS). The exact etiology MS development unclear, but various environmental and genetic factors might play role initiating disease. Experimental encephalomyelitis (EAE) mouse model used to study pathophysiology as well effects possible therapeutic agents. In addition...
UNLABELLED microRNA-155 (miR-155) plays an important role in posttranscriptional gene regulation of the immune system. We and others have described miR-155 upregulation in T helper cells (Th) during the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. We have shown that mice in which the miR-155 host gene (MIR155HG) has been deactivated are ...
Apoptosis signal-regulating kinase 1 (ASK1) is an evolutionarily conserved mitogen-activated protein kinase (MAPK) kinase kinase which plays important roles in stress and immune responses. Here, we show that ASK1 deficiency attenuates neuroinflammation in experimental autoimmune encephalomyelitis (EAE), without affecting the proliferation capability of T cells. Moreover, we found that EAE upreg...
The article by Johnson et al. on the role of antioxidant signaling pathways in a model of experimental autoimmune encephalomyelitis (EAE) merits further discussion. This group hypothesized that alterations in oxidative signaling may be involved in the development of EAE and multiple sclerosis (MS). Their laboratory has performed extensive characterization of the nuclear factor erythroid 2-relat...
Potent immunosuppressive and regenerative properties of mesenchymal stem cells (MSCs) position them as a novel therapy for autoimmune diseases. This research examines the therapeutic effect of MSCs administration at different disease stages in experimental autoimmune encephalomyelitis (EAE). Classical and atypical scores of EAE, associated with Th1 and Th17 response, respectively, and also Treg...
Multiple sclerosis (MS) is a chronic debilitating disease affecting the central nervous system (CNS) in humans. Experimental autoimmune encephalomyelitis (EAE) remains the primary animal model of MS. MS/EAE are considered to be autoimmune diseases mediated by CD4 T helper (TH) cells. The role of B cells and antibody is under debate. Previous studies established B cell dependent (induced with re...
Experimental allergic encephalomyelitis (EAE), a demyelinating disease induced in the animals parallels multiple sclerosis in human in several aspects, provides a useful model to investigate multiple sclerosis. In this study, we have therefore used this model to study functions of nerve growth factor (NGF) in EAE. NGF with considerable effects on neuron survival, proliferation and differentiati...
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