medigraphic.com
Academia Mexicana de Neurología, A.C.

2006, Número 6

<< Anterior Siguiente >>

Rev Mex Neuroci 2006; 7 (6)


Apuntes sobre mecanismos inmunopatológicos en el síndrome de Guillain-Barré

Cardoso-Suárez T, Robinson-Agramonte MÁ

Idioma: Español
Referencias bibliográficas: 30
Paginas: 599-603
Archivo PDF: 137.04 Kb.


RESUMEN

Las enfermedades desmielinizantes se caracterizan por ser procesos inflamatorios adquiridos, que afectan selectivamente la mielina del tejido nervioso central y periférico. Su ocurrencia en humanos incluye una variedad de procesos inflamatorios agudos y subagudos, entre los que se encuentran: la neuromielitis óptica, encefalomielitis diseminada aguda y la polirradiculoneuropatía inflamatoria aguda o síndrome de Guillain-Barré (SGB). El mimetismo molecular entre agentes ambientales como C. jejuni y moléculas de nervios periféricos parece ser un elemento importante en la producción de esta enfermedad de perfil autoinmune. Quedan interrogantes como por qué en el SGB el daño axonal y de la mielina queda restringido al SNP y otras como el papel de los linfocitos T en la patogénesis del SGB.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Lucchinetti C. The spectrum of idiopathic inflammatory demyelinating disease. Am Academy of Neurology. Syllabi on CD ROM. 2000. Ref Type: Electronic Citation.

  2. Onuki M, Ayers MM, Bernard CC, Orian JM. Axonal degeneration is an early pathological feature in autoimmune-mediated demyelination in mice. Microsc Res Tech 2001; 52: 731-9.

  3. Ho TW, et al. Human autoimmune neuropathies. Annu Rev Neurosci 1998; 21: 187-226.

  4. Stojkovic T, Dubucquoi S. The use of intravenous immunoglobulins in neurology. Rev Neurol (Paris) 2005; 161: 781-94.

  5. Van Doorn PA. Treatment of Guillain-Barre syndrome and CIDP. J Peripher Nerv Syst 2005; 10: 113-27.

  6. Green DM. Advances in the management of Guillain-Barre syndrome. Curr Neurol Neurosci Rep 2002; 2: 541-8.

  7. Zhang G, et al. Anti-ganglioside antibody-mediated neuronal cytotoxicity and its protection by intravenous immunoglobulin: implications for immune neuropathies. Brain 2004; 127: 1085-100.

  8. Hadden RD, Cornblath DR, Hughes RA. Electrophysiological classification of Guillain-Barré syndrome: a reappraisal. Ann Neurol 1998; 44: 780-8.

  9. Hughes RA, Cornblath DR. Guillain-Barre syndrome. Lancet 2005; 366: 1653-66.

  10. Guillain-Barre syndrome: an Italian multicentre case-control study. Guillain-Barre Syndrome Study Group. Neurol Sci 2000; 21: 229-34.

  11. McCarthy N, Giesecke J. Incidence of Guillain-Barre syndrome following infection with Campylobacter jejuni. Am J Epidemiol 2001; 153: 610-14.

  12. Haber P, et al. Guillain-Barre syndrome following influenza vaccination. JAMA 2004; 292: 2478-81.

  13. Ogawara K, et al. Anti-GM1b IgG antibody is associated with acute motor axonal neuropathy and Campylobacter jejuni infection. J Neurol Sci 2003; 210: 41-5.

  14. Kuwabara S, et al. Differences in membrane properties of axonal and demyelinating Guillain-Barre syndromes. Ann Neurol 2002; 52: 180-7.

  15. Goodfellow JA, et al. Overexpression of GD1a ganglioside sensitizes motor nerve terminals to anti-GD1a antibody-mediated injury in a model of acute motor axonal neuropathy. J Neurosci 2005; 25: 1620-8.

  16. Kuwabara S, et al. Does Campylobacter jejuni infection elicit «demyelinating» Guillain-Barre syndrome? Neurology 2004; 63: 529-33.

  17. Willison HJ, Yuki N. Peripheral neuropathies and anti-glycolipid antibodies. Brain 2002; 125: 2591-625.

  18. Kwa MS, et al. Autoimmunoreactivity to Schwann cells in patients with inflammatory neuropathies. Brain 2003; 126: 361-75.

  19. Hafer-Macko, CE, et al. Immune attack on the Schwann cell surface in acute inflammatory demyelinating polyneuropathy. Ann Neurol 1996; 39: 625-35.

  20. Yuki N, et al. Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain-Barre syndrome. Proc Natl Acad Sci USA 2004; 101: 11404-9.

  21. Gabriel CM, Hughes RAC, Moore SE, Walsh FS. Induction of experimental neuritis with peripheral myelin protein 22. Brain 1998; 121: 1895-902.

  22. Putzu GA, et al. Immunohistochemical localization of cytokines, C5b-9 and ICAM-1 in peripheral nerve of Guillain-Barre syndrome. J Neurol Sci 2000; 174: 16-21.

  23. Creange A, et al. Matrix metalloproteinase-9 is increased and correlates with severity in Guillain-Barre syndrome. Neurology 1999; 53: 1683-91.

  24. Sharshar T, et al. MMP-9 correlates with electrophysiologic abnormalities in Guillain-Barre syndrome. Neurology 2002; 59: 1649-51.

  25. Ang CW, Jacobs BC, Laman JD. The Guillain-Barre syndrome: a true case of molecular mimicry. Trends Immunol 2004; 25: 61-6.

  26. Gong Y, et al. Localization of major gangliosides in the PNS: implications for immune neuropathies. Brain 2002; 125: 2491-506.

  27. Godschalk PC, et al. The crucial role of Campylobacter jejuni genes in anti-ganglioside antibody induction in Guillain-Barre syndrome. J Clin Invest 2004; 114: 1659-65.

  28. Yuki N, Odaka M, Ganglioside mimicry as a cause of Guillain-Barre syndrome. Curr Opin Neurol 2005; 18: 557-61.

  29. Cavanna B, et al. Anti-GM(2) IgM antibody-induced complement-mediated cytotoxicity in patients with dysimmune neuropathies. J Neuroimmunol 2001; 114: 226-31.

  30. Wanschitz J, Maier H, Lassmann H, Budka H, Berger T. Distinct time pattern of complement activation and cytotoxic T cell response in Guillain-Barre syndrome. Brain 2003; 126: 2034-42.




2020     |     www.medigraphic.com