Commentary Open Access
Volume 1 | Issue 3 | DOI: https://doi.org/10.33696/Neurol.1.017

Neurocysticercosis: Autoantibodies, Another Cog in the Wheel of Its Variable Pathogenicity

  • 1Institute Gulbenkian de Ciencia, 6, Rua Quinta Grande, Oeiras 2780-156, Oeiras, Portugal
  • 2Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México D.F. 04510, Mexico
  • 3Instituto de Investigaciones Biomédicas “Dr. Francisco J. Triana-Alonso”, (BIOMED-UC) Facultad de Ciencias de la Salud, Sede Aragua, Universidad de Carabobo, Av. Las Delicias, Maracay, PO Box: 2351, Aragua, Venezuela
  • 4Unidad de Neuroinflamación (Instituto de Investigaciones Biomédicas-UNAM, Instituto Nacional de Neurología y Neurocirugía,Facultad de Medicina-UNAM), Insurgentes Sur 3877, Colonia La Fama, delegación Tlalpan, México D.F, México; Neurocysticercosis Clinic, Instituto Nacional de Neurología y Neurocirugía, México D.F, México
  • 5School of Medicine, University of Cuenca, Av. 12 de Abril y Av. Loja Cuenca, Ecuador
  • 6G. H. Sergievsky Center, Columbia University, New York, New York, USA
+ Affiliations - Affiliations

Corresponding Author

R Michael E Parkhouse, parkhous@igc.gulbenkian.pt,

 Arturo Carpio, arturo.carpio@ ucuenca.edu.ec

Received Date: July 15, 2020

Accepted Date: July 31, 2020


Neurocysticercosis (NC) presents a spectrum of clinical symptoms, with two broad clinical entities based on the CNS location of the parasite: parenchymal (P-NC) or extraparenchymal (EP-NC). In view of the importance of inflammation in the pathogenesis of NC, it is surprising that the possible occurrence of anti-brain autoantibodies in NC has not been explored until recently. In this study the presence of autoantibodies to nine ubiquitous intracellular proteins from extraparenchymal (EP-NC) was reported. Levels of these autoantibodies were greatly reduced or absent in P-NC, an observation consistent with our understanding of the immunological potential of these two distinct anatomical areas of the brain. In more recent work, we similarly observed autoantibodies to tubulin and MOG in the CSF of EP-NC, but not P-NC patients. In addition to the evident importance of the early inflammatory response, the identification of autoantibodies to the neuronal surface protein MOG (and perhaps other anti-neuronal autoantibodies) provides a potentially critical role in the pathogenesis of NC through their predicted potential for antibody mediated cytotoxicity and the subsequent release of intracellular proteins which, in turn, would stimulate a cascade of more autoantibodies to the liberated intracellular proteins. These, together with antibodies to metacestode proteins may be expected to play an important role in the continuously evolving and variable pathogenesis of NC, as is summarized in the hypothetical model presented.



Neurocysticercosis; Anti-brain autoantibodies; Tubulin; MOG; Extraparenchymal; Parenchymal

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