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J Neuroimmunol. 2015 Dec 15;289:8-11. doi: 10.1016/j.jneuroim.2015.10.007. Epub 2015 Oct 13. Alexopoulos H1, Kampylafka EI1, Fouka P2, Tatouli I1, Akrivou S1, Politis PK3, Moutsopoulos HM1,…
Fazio R et al. – Neuromyelitis optica (NMO) is a rare demyelinating disease, affecting selectively the optic nerve and the spinal cord. It was previously considered to be a severe variant of multiple sclerosis (MS) due to the similar pathological features and its resemblance to optico–spinal, or Japanese, MS, typical of Asian populations.
Interleukin-17 (IL-17) secreted by T helper 17 (Th17) cells is essential in the development of experimental autoimmune encephalomyelitis (EAE). However, it remains unclear how IL-17-mediated signaling in different cellular compartments participates in the central nervous system (CNS) inflammatory process.
Background: Neuromyelitis optica (NMO) is characterized by severe optic neuritis and transverse myelitis. A disease-specific autoantibody against aquaporin (AQP) 4, mainly expressed in astrocytic foot processes, was found in the sera from patients with NMO.
Reactive astrogliosis, whereby astrocytes undergo varying molecular and morphological changes, is a ubiquitous but poorly understood hallmark of all central nervous system pathologies. Genetic tools are now enabling the molecular dissection of the functions and mechanisms of reactive astrogliosis in vivo. Recent studies provide compelling evidence that reactive astrogliosis can exert both beneficial and detrimental effects in a context-dependent manner determined by specific molecular signaling cascades
Background: NMO-IgG autoantibody is now considered a useful serum biomarker of neuromyelitis optica (NMO). A series of clinical and pathological observations suggest that NMO-IgG may play a central role in NMO physiopathology. Objective: The aim of this in vitro-based study was to characterize molecular and functional consequences of interaction between NMO-IgG and primary cultures of astrocytes.