We present a patient with benign IgM-lambda anti-Sulfatide (SUL) whose
neuropathy was transferred in newborn rabbits. The patient's clinico-
pathological picture of anti-SUL-associated demyelinating neuropathy i
s reported. The monoclonal IgM antibodies prepared by Tatum's method,
that retained their biological activity, were passively transferred to
newborn rabbits. The passive transfer produced demyelinating nerve le
sions very similar to the donor antibody neuropathy. In experimental l
esions we observed the human IgM anti-SUL antibodies binding to Schmid
t-Lanterman incisures and nodes of Ranvier. We postulate that the myel
in-specific and complement-dependent lesions observed in the periphera
l nerve support the potential demyelinating role of anti-SUL antibodie
s. Moreover, the pattern of the antibody binding to the perineuronal s
heath of satellite cells in dorsal root ganglia strengthen the hypothe
sis that anti-SUL antibodies may have a pathogenetic role in this sens
orimotor syndrome.