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.
Bibliographical noteFunding Information:
This research was supported by grants from The Association Française contre les Myopathies and The Muscular Dystrophy Association of America.
Copyright 2006 Elsevier B.V., All rights reserved.
- Costimulatory molecules
- Experimental autoimmune myasthenia gravis
- Nasal tolerance