Passively transferred myasthenia gravis: protection of mouse endplates by Fab fragments from human myasthenic IgG.
AUTOR(ES)
Toyka, K V
RESUMO
Using the mouse passive transfer model, the effects of purified human myasthenic immunoglobulin G and of the monovalent Fab fragment on neuromuscular junctions were investigated. Treatment with IgG markedly reduced amplitudes of miniature endplate potentials. When Fab fragments were transferred alone or with subsequent addition of IgG no neuromuscular transmission block was induced. Myasthentic IgG and Fab were specifically demonstrated at the neuromuscular junctions by immunohistochemistry. On electronmicroscopy endplate structure was normal in transfer experiments using IgG for up to 30 days. It is suggested that Fab fragments bind to acetylcholine receptors without affecting transmission and protect them from the attack of complete IgG antibodies.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=490676Documentos Relacionados
- Prevention of passively transferred experimental autoimmune myasthenia gravis by a phage library-derived cyclic peptide
- Acetylcholine receptor turnover in mice with passively transferred myasthenia gravis. I. Receptor degradation.
- Acetylcholine receptor turnover in mice with passively transferred myasthenia gravis. II. Receptor synthesis.
- High avidity IFN-neutralizing antibodies in pharmaceutically prepared human IgG.
- Amplification of IgG VH and VL (Fab) from single human plasma cells and B cells
