Cross‐reactivity of anti‐galactocerebroside autoantibodies with a Trypanosoma brucei proteolipidic epitope

Pathogenic mechanisms of the demyelinating encephalopathy featuring the nervous phase of human African trypanosomiasis (HAT) are largely unknown. They might include autoimmune disorders. A variety of autoantibodies is detected during the disease and we have previously evidenced anti‐galactocerebroside (GalC) antibodies in the serum and cerebrospinal fluid (CSF) from patients in the nervous stage (stage II) of HAT. We now show that anti‐GalC antibodies recognize an antigen located on the parasite membrane and common to different strains of trypanosomes. By using affinity chromatography with a rabbit anti‐GalC antiserum, a 52‐kD proteolipid was isolated from the membrane of Trypanosoma brucei ( T. b .) brucei AnTat 1.9, AnTat 1.1E, and T. b. rhodesiense Etat 1.2/R and Etat 1.2/S. Antibodies directed against this antigen were found in the CSF from patients with nervous stage HAT. These CSF also contained anti‐GalC antibodies and adsorption with the proteolipid decreased anti‐GalC reactivity. Immunization of mice with this antigen induced the production of antibodies which cross‐reacted with GalC but no protection from experimental infection with T. b. brucei . These data support the hypothesis that anti‐GalC antibodies detected in the CSF from HAT patients might be induced by molecular mimicry with a parasite antigen.