dc.creatorParkhouse, Michael
dc.creatorSciutto, Edda
dc.creatorHernández, Marisela
dc.creatorCortez, Maria
dc.creatorCarpio Rodas, Luis Arturo
dc.creatorFleury, Agnes
dc.date.accessioned2021-01-12T17:24:27Z
dc.date.accessioned2022-10-20T20:45:23Z
dc.date.available2021-01-12T17:24:27Z
dc.date.available2022-10-20T20:45:23Z
dc.date.created2021-01-12T17:24:27Z
dc.date.issued2020
dc.identifier01655728, e 1872-8421
dc.identifierhttps://www.scopus.com/record/display.uri?eid=2-s2.0-85091217062&doi=10.1016%2fj.jneuroim.2020.577389&origin=inward&txGid=831beafae4a0d5a058f83bc579e79f18
dc.identifier10.1016/j.jneuroim.2020.577389
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/4598658
dc.description.abstractNeurocysticercosis (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
dc.languagees_ES
dc.sourceJournal of Neuroimmunology
dc.subjectNeurocysticercosis
dc.subjectAnti-brain autoantibodies
dc.subjectTubulin
dc.subjectMOGHP10
dc.subjectExtraparenchymal
dc.subjectParenchymal
dc.titleExtraparenchymal human neurocysticercosis induces autoantibodies against brain tubulin and MOG35–55 in cerebral spinal fluid
dc.typeARTÍCULO


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