Mechanism of nasal tolerance induced by a recombinant fragment of acetylcholine receptor for treatment of experimental myasthenia gravis

Sin Hyeog Im, Dora Barchan, Sara Fuchs, Miriam Souroujon

Research output: Contribution to journalArticlepeer-review

Abstract

Acetylcholine receptor (AChR) is the major autoantigen in myasthenia gravis (MG) and experimental autoimmune MG (EAMG). Here we analyze the mechanisms involved in suppression of ongoing EAMG in rats by nasal administration of a recombinant fragment from the human AChR α-subunit. We demonstrate that such a fragment, expressed without a fusion partner, confers nasal tolerance that can be adoptively transferred. Our observations suggest that the underlying mechanism of this nasal tolerance is active suppression involving a shift from a Th1 to a Th2/Th3-regulated AChR-specific response which may be mediated by down regulation of costimulatory factors. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)161-168
Number of pages8
JournalJournal of Neuroimmunology
Volume111
Issue number1-2
DOIs
StatePublished - 1 Nov 2000

Bibliographical note

Funding Information:
This research was supported by grants from The Association Française contre les Myopathies and The Muscular Dystrophy Association of America.

Copyright:
Copyright 2006 Elsevier B.V., All rights reserved.

Keywords

  • Costimulatory molecules
  • Experimental autoimmune myasthenia gravis
  • Immunotherapy
  • Nasal tolerance
  • Th1/Th2

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