Neuromyelitis Optica Spectrum Disorder (NMOSD) is characterized as an autoimmune, inflammatory and demyelinating disease of the Central Nervous System (CNS). Its pathogenesis is due to the presence of anti-aquaporin 4 immunoglobulin G1 antibodies (anti-AQP4IgG), with presence of lymphocytes T Helper 1 and 17 (TH1 and TH17), in addition to previous neuroinflammation. The Mast cell (MC) is a granular cell present in all vascularized tissues, close to vessels, nerves, and meninges. In CNS, MCs are in the area postrema, choroid plexus, thalamus and hypothalamus. MC has ability to transmigrate between the nervous tissue and the lymphoid organs, interacting with the cells of both systems. These cells reach the CNS during development through vessel migration. Most MCs reside on the abluminal side of the vessels, where it can communicate with neurons, glial cells, endothelial cells and the extracellular matrix. Considering the role of MCs in neurodegenerative diseases has been extensively discussed, we hypothesized MCs participate in the pathogenesis of NMOSD. This cell represents an innate and adaptive immune response regulator, capable of faster responses than microglial cells. The study of MCs in NMOSD can help to elucidate the pathogenesis of this disease and guide new research for the treatment of patients in the future. We believe this cell is an important component in the cascade of NMOSD neuroinflammation.
Keywords: Demyelinating diseases; Immune response and neuroinflammation; Mast cells (MCs); Neuromyelitis optica syndrome disorder (NMOSD).
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