neuromyelitis optica/tyrosine

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Glatiramer acetate could be a hypothetical therapeutic agent for neuromyelitis optica.

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Neuromyelitis optica (NMO) is characterized by concurrence of optic neuritis and transverse myelitis, which is typically associated with a spinal cord lesion extending three or more vertebral segments. NMO is an inflammatory, demyelinating central nervous system disorder, and although it has a

Type I interferon signature is high in lupus and neuromyelitis optica but low in multiple sclerosis.

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OBJECTIVE Neuromyelitis optica (NMO) is characterized by selective inflammation of the spinal cord and optic nerves but is distinct from multiple sclerosis (MS). Interferon (IFN)-β mitigates disease activity in MS, but is controversial in NMO, with a few reports of disease worsening after IFN-β

HLA, PTPN22 and PD-1 associations as markers of autoimmunity in neuromyelitis optica.

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BACKGROUND Neuromyelitis optica (NMO) is a disease with autoimmune characteristics. A genetic autoimmune dependency for NMO has not been clarified in detail. OBJECTIVE To investigate immunogenetic aspects of NMO. METHODS Forty-one patients with NMO and 42 patients with multiple sclerosis (MS) were

High levels of antibodies against PtpA and PknG secreted by Mycobacterium avium ssp. paratuberculosis are present in neuromyelitis optica spectrum disorder and multiple sclerosis patients.

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Mycobacterium avium ssp. paratuberculosis (Map) is the etiological agent of Paratuberculosis in ruminants. Protein tyrosine phosphatase A (PtpA) and protein kinase G (PknG) are secreted proteins necessary for the survival of the pathogen within macrophages. In this study we analyzed if Map was able

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