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Harmful effects of anti-GalNAc-GD1a antibodies and TNF-α on rat dorsal root ganglia

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The clinical characteristics of five (22%) of 23 patients with Guillain‐Barré syndrome (GBS), whose serum contained immunoglobulin G (IgG) antibodies to the ganglioside N-acetylgalactosaminyl GD1a (GalNAc-GD1a), included pure motor weakness of the axonal type. These patients had a relatively good prognosis, but displayed higher serum tumor necrosis factor-alpha (TNF-α) titers than the other GBS patients. We examined the effect of serum from these patients with IgG anti-GalNAc-GD1a antibodies on neurites from cultured rat dorsal root ganglia (DRG) and found it to damage the myelin in well-elongated DRG neurites and monolayer cultures of Schwann cells and neurons. In the regeneration model, serum from these patients delayed neurite extension and inhibited Schwann cell proliferation. Neurons in cultured monolayers showed vacuolation and decreased rapidly in number. Schwann cells were also vacuolated and readily detached from the substratum. The effects of IgG anti-GalNAc-GD1a antibodies purified from one of the patients, rabbit serum after immunization with GalNAc-GD1a, and recombinant TNF-α were also examined. IgG anti-GalNAc-GD1a antibodies mainly inhibited the regeneration and preservation of neurons, while TNF-α mainly induced morphological changes in well-proliferated Schwann cells and myelin.
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Keywords: IgG anti-GalNAc-GD1a antibody; TNF-α; axonal type Guillain‐Barré syndrome; dorsal root ganglia

Document Type: Research Article

Affiliations: 1: Third Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama; 2: Department of Neurology, School of Medicine, Kinki University, Osaka; and 3: Laboratory of Molecular and Cellular Physiology, National Defense Medical College, Tokorozawa, Saitama, Japan

Publication date: June 1, 2005

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