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Anti-GM1 antibody facilitates leakage in an in vitro blood–nerve barrier model

From the Department of Neurology and Neuroscience (Drs. Kanda, Iwasaki, Yamawaki, and Mizusawa), Tokyo Medical and Dental University Graduate School of Medicine; and the Department of Tumor Immunology (Dr. Tai), Tokyo Metropolitan Institute of Medical Sciences, Japan.

Address correspondence and reprint requests to Dr. Takashi Kanda, Department of Neurology and Neuroscience, Tokyo Medical and Dental University Graduate School of Medicine, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan; e-mail: t-kanda.nuro{at}med.tmd.ac.jp

Using an in vitro blood–nerve barrier (BNB) model, the authors tested the effect of various monoclonal antiganglioside antibodies on BNB function. Only anti-GM1 antibody significantly facilitated BNB leakage in a concentration-dependent, complement-independent manner. This study provided evidence that anti-GM1 antibody, frequently detected in sera from patients with inflammatory neuropathies, may participate BNB dysfunction and contribute to development of neuropathy.

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