Conclusion: MOG antibodies are found across a variety of pediatric demyelinating syndromes having some distinct clinical and MRI features. (Source: Multiple Sclerosis)
γδ (gamma delta) T cells, a small population of unconventional T cells, have been seen in central nervous system (CNS) lesions of multiple sclerosis (MS) patients, but their function in disease activity is not clearly understood.
Journal of Neuroinflammation is an open access, peer-reviewed journal that focuses on innate immunological responses of the nervous system, involving microglia, astrocytes, cytokines, chemokines, complement proteins, acute phase proteins,...
People who take the drug natalizumab for multiple sclerosis may have up to a 10 times greater risk of developing a risk biomarker for activity of a virus that can lead to an often fatal brain disease, according to a study ...
The choroid plexus is a villous epithelial–endothelial vascular structure located within the ventricular system and is primarily responsible for the production of CSF.
Recent findings have revealed distinct roles for type I and II interferons (IFN-I and IFN-γ) in the recruitment of immune cells to the central nervous system (CNS) and highlighted the importance of this process for brain maintenance and...
Blood-borne monocyte derived cells play a pivotal, initially unrecognized, role in most central nervous system disorders, including diseases initially classified as purely neurodegenerative (i.e. AD, PD, and ALS).
Extracellular vesicles, namely exosomes and shed vesicles, are released by virtually any cell type and can be detected and identified in terms of cell origin in biological fluids. They therefore constitute an ideal tool to access information on cells residing in an inaccessible site such as the brain. We will review here available information on extracellular vesicles detection in neurological disorders with special emphasis on neurodegenerative diseases.
... We report that both D13 and ICSM18 induce rapid, dose-dependent, on-target neurotoxicity. We conclude that antibodies directed to this region may not be suitable as therapeutics. No such toxicity was found when antibodies against the flexible tail of PrPCwere administered. Any attempt at immunotherapy or immunoprophylaxis of prion diseases should account for these potential untoward effects.
Kuti Baruch,Aleksandra Deczkowska,Neta Rosenzweig,Afroditi Tsitsou-Kampeli,Alaa Mohammad Sharif,Orit Matcovitch-Natan,Alexander Kertser,Eyal David,Ido Amit&Michal SchwartzAffiliationsContributionsCorresponding authorsNature Medicine (2016) doi:10.1038/nm.4022Received 12 October 2015 Accepted 04 December 2015 Published online 18 January 2016
Systemic immune suppression may curtail the ability to mount the protective, cell-mediated immune responses that are needed for brain repair. By using mouse models of Alzheimer's disease (AD), we show that immune checkpoint blockade directed against the programmed death-1 (PD-1) pathway evokes an interferon (IFN)-γ–dependent systemic immune response, which is followed by the recruitment of monocyte-derived macrophages to the brain. When induced in mice with established pathology, this immunological response leads to clearance of cerebral amyloid-β (Aβ) plaques and improved cognitive performance. Repeated treatment sessions were required to maintain a long-lasting beneficial effect on disease pathology. These findings suggest that immune checkpoints may be targeted therapeutically in AD.
Background Typical and atypical optic neuritis (ON) are two clinical types of autoimmune inflammatory diseases of the optic nerve that causes acute vision loss, and are difficult to distinguish in their early stages.
Hematopoietic stem cell transplantation (HSCT) is a treatment paradigm that has long been utilized for cancers of the blood and bone marrow but has gained some traction as a treatment paradigm for multiple sclerosis (MS).
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