Conduction failure and nerve conduction slowing in experimental allergic neuritis induced by P2-specific T-cell lines

Authors

  • Kurt Heininger MD, PhD,

    1. Department of Neurology, University of Düsseldorf, and the Max-Planck Society, Clinical Research Unit for Multiple Sclerosis, Würzburg, Federal Republic of Germany
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  • Guido Stoll MD,

    1. Department of Neurology, University of Düsseldorf, and the Max-Planck Society, Clinical Research Unit for Multiple Sclerosis, Würzburg, Federal Republic of Germany
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  • Christopher Linington PhD,

    1. Department of Neurology, University of Düsseldorf, and the Max-Planck Society, Clinical Research Unit for Multiple Sclerosis, Würzburg, Federal Republic of Germany
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  • Dr Klaus V. Toyka MD,

    Corresponding author
    1. Department of Neurology, University of Düsseldorf, and the Max-Planck Society, Clinical Research Unit for Multiple Sclerosis, Würzburg, Federal Republic of Germany
    • Neurologische Klinik der Universität, Moorenstr. 5, 4000 Düsseldorf, Federal Republic of Germany
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  • Hartmut Wekerle MD

    1. Department of Neurology, University of Düsseldorf, and the Max-Planck Society, Clinical Research Unit for Multiple Sclerosis, Würzburg, Federal Republic of Germany
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Abstract

P2-specific T cells (LiP2/A) mediate experimental allergic neuritis (EAN) in the Lewis rat after adoptive transfer to naive recipients. After a latent period of 4 days, injection of 2 × 106 line cells induced fulminant paraplegia and complete conduction failure in the peripheral nerves and roots, resembling acute axonal breakdown. Injection with 106 cells caused milder clinical signs, nerve conduction failure, and conduction slowing. Clinical and electrophysiological recovery from adoptively transferred EAN was nearly complete and its time course was inversely correlated to the initial severity of EAN. These findings suggest that EAN induced by the P2-specific T-cell line can lead to a profound and rapidly evolving nerve dysfunction in a dose-dependent fashion.

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