T. Ohsawa et al., ANTI-B-SERIES GANGLIOSIDE-RECOGNIZING AUTOANTIBODIES IN AN ACUTE SENSORY NEUROPATHY PATIENT CAUSE CELL-DEATH OF RAT DORSAL-ROOT GANGLION NEURONS, Neuroscience letters, 157(2), 1993, pp. 167-170
To examine the cytotoxicity of a patient's serum with an acute relapsi
ng sensory neuropathy syndrome, dorsal root ganglion neurons from youn
g adult rats were cultured in the presence of the patient's serum whic
h had an extremely higher-titer monoclonal IgM antibody recognizing B-
series gangliosides, GD2, GD1b, GT1b and GQ1b. By the addition of the
inactivated patient's serum, the relatively larger cells died after un
dergoing of metamorphosis during several hours of culture, whilst the
smaller cells survived. The IgM fraction isolated from the patient's s
erum showed similar cytotoxicity towards the neurons as the inactivate
d whole serum. No cytotoxicity was observed with the IgM fraction-cont
aining medium after it had been absorbed with ganglioside GD1b. The re
sults suggested that the anti-B-series ganglioside-directed antibody i
s the causal agent for the human neurologic disease.