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Title: Extraparenchymal human neurocysticercosis induces autoantibodies against brain tubulin and MOG35–55 in cerebral spinal fluid
Authors: Parkhouse, Michael
Sciutto, Edda
Hernández, Marisela
Cortez, Maria
Carpio Rodas, Luis Arturo
Fleury, Agnes
metadata.dc.ucuenca.correspondencia: Parkhouse, Michael, parkhous@igc.gulbenkian.pt
Keywords: Neurocysticercosis
Anti-brain autoantibodies
Tubulin
MOGHP10
Extraparenchymal
Parenchymal
metadata.dc.ucuenca.areaconocimientofrascatiamplio: 3. Ciencias Médicas y de la Salud
metadata.dc.ucuenca.areaconocimientofrascatidetallado: 3.3.9 Enfermedades Infecciosas
metadata.dc.ucuenca.areaconocimientofrascatiespecifico: 3.3 Ciencias de la Salud
metadata.dc.ucuenca.areaconocimientounescoamplio: 09 - Salud y Bienestar
metadata.dc.ucuenca.areaconocimientounescodetallado: 0912 - Medicina
metadata.dc.ucuenca.areaconocimientounescoespecifico: 091 - Salud
Issue Date: 2020
metadata.dc.ucuenca.volumen: Volumen 349
metadata.dc.source: Journal of Neuroimmunology
metadata.dc.identifier.doi: 10.1016/j.jneuroim.2020.577389
metadata.dc.type: ARTÍCULO
Abstract: 
Neurocysticercosis (NC) presents two broad clinical entities: extraparenchymal (EP-NC) and parenchymal (P-NC). Using ELISA methodology, we demonstrate autoantibodies to tubulin and the Major oligodendrocyte glycoprotein (MOG) in the CSF of most, but not all, EP-NC samples. Levels of these autoantibodies were considerably reduced or absent in the P-NC samples. There was a striking correlation between levels of anti-tubulin and anti-MOG, and the significant correlation between the levels of autoantibodies and cellularity in the CSF, suggests that stimulation of the autoantibody response may be a function of cerebral inflammation. A hypothetical model to describe the pathogenesis of EP-NC is presented
URI: https://www.scopus.com/record/display.uri?eid=2-s2.0-85091217062&doi=10.1016%2fj.jneuroim.2020.577389&origin=inward&txGid=831beafae4a0d5a058f83bc579e79f18
metadata.dc.ucuenca.urifuente: https://www.sciencedirect.com/journal/journal-of-neuroimmunology/vol/349/suppl/C
ISSN: 01655728, e 1872-8421
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