Using an in vitro blood-nerve barrier (BNB) model, the authors tested the e
ffect of various monoclonal antiganglioside antibodies on BNB function. Onl
y anti-GM1 antibody significantly facilitated BNB leakage in a concentratio
n-dependent, complement-independent manner. This study provided evidence th
at anti-GM1 antibody, frequently detected in sera from patients with inflam
matory neuropathies, may participate BNB dysfunction and contribute to deve
lopment of neuropathy.