info:eu-repo/semantics/article
Experimental Guillain-Barre syndrome induced by immunization with gangliosides: Keyhole limpet hemocyanin is required for disease triggering
Fecha
2017-06Registro en:
Funes, Samanta Celeste; Chiari, Maria Eugenia; Comin, Romina; Irazoqui, Fernando Jose; Nores, Gustavo Alejandro; Experimental Guillain-Barre syndrome induced by immunization with gangliosides: Keyhole limpet hemocyanin is required for disease triggering; Elsevier Science; Biochimica et Biophysica Acta - Molecular Basis of Disease; 1863; 6; 6-2017; 1473-1478
0925-4439
CONICET Digital
CONICET
Autor
Funes, Samanta Celeste
Chiari, Maria Eugenia
Comin, Romina
Irazoqui, Fernando Jose
Nores, Gustavo Alejandro
Resumen
An experimental model of Guillain-Barré Syndrome has been established in recent years. Rabbits develop disease upon immunization with a single dose of an emulsion containing bovine brain gangliosides, KLH and complete Freund's adjuvant. Within a period of four to ten weeks after immunization, they began to produce anti-ganglioside IgG-antibodies first, and to show clinical signs of neuropathy afterwards. In addition to gangliosides, KLH is a requirement for antibody production and disease triggering. Although KLH is commonly used as an immunological carrier protein, an anti-KLH-specific immune response was necessary for induction of both events. KLH is a glycoprotein carrying most of the immunogenicity in its glycan moiety. Between 20% to 80% of anti-ganglioside IgG-antibodies present in sick rabbit sera cross-reacted with KLH, indicating that both immune responses are related. The terminal Gal-ß(1,3)-GalNAc glycan (present in gangliosides and KLH) is proposed as “key” antigenic determinant involved in inducing the anti-ganglioside immune response. These results are discussed in the context of the “binding site drift” hypothesis.