M. Girard et al., Cross-reactivity of anti-galactocerebroside autoantibodies with a Trypanosoma brucei proteolipidic epitope, CLIN EXP IM, 119(3), 2000, pp. 516-522
Pathogenic mechanisms of the demyelinating encephalopathy featuring the ner
vous phase of human African trypanosomiasis (HAT) are largely unknown. They
might include autoimmune disorders. A variety of autoantibodies is detecte
d during the disease and we have previously evidenced anti-galactocerebrosi
de (GalC) antibodies in the serum and cerebrospinal fluid (CSF) from patien
ts in the nervous stage (stage II) of HAT. We now show that anti-GalC antib
odies recognize an antigen located on the parasite membrane and common to d
ifferent strains of trypanosomes. By using affinity chromatography with a r
abbit anti-GalC antiserum, a 52-kD proteolipid was isolated from the membra
ne of Trypanosoma brucei (T. b.) brucei AnTat 1.9, AnTat 1.1E, and T. b. rh
odesiense Etat 1.2/R and Etat 1.2/S. Antibodies directed against this antig
en were found in the CSF from patients with nervous stage HAT. These CSF al
so contained anti-GalC antibodies and adsorption with the proteolipid decre
ased anti-GalC reactivity. Immunization of mice with this antigen induced t
he production of antibodies which cross-reacted with GalC but no protection
from experimental infection with T. b. brucei. These data support the hypo
thesis that anti-GalC antibodies detected in the CSF from HAT patients migh
t be induced by molecular mimicry with a parasite antigen.