Im_1999_J.Clin.Invest_104_1723

Reference

Title : Suppression of ongoing experimental myasthenia by oral treatment with an acetylcholine receptor recombinant fragment - Im_1999_J.Clin.Invest_104_1723
Author(s) : Im SH , Barchan D , Fuchs S , Souroujon MC
Ref : J Clinical Investigation , 104 :1723 , 1999
Abstract :

Myasthenia gravis (MG) is an autoimmune disorder in which the nicotinic acetylcholine receptor (AChR) is the major autoantigen. In an attempt to develop an antigen-specific therapy for MG, we administered a nonmyasthenogenic recombinant fragment of AChR orally to rats. This fragment, corresponding to the extracellular domain of the human AChR alpha-subunit (Halpha1-205), protected rats from subsequently induced experimental autoimmune myasthenia gravis (EAMG) and suppressed ongoing EAMG when treatment was initiated during either the acute or chronic phases of disease. Prevention and suppression of EAMG were accompanied by a significant decrease in AChR-specific humoral and cellular responses. The underlying mechanism for the Halpha1-205-induced oral tolerance seems to be active suppression, mediated by a shift from a T-helper 1 (Th1) to a Th2/Th3 response. This shift was assessed by changes in the cytokine profile, a deviation of anti-AChR IgG isotypes from IgG2 to IgG1, and a suppressed AChR-specific delayed-type hypersensitivity response. Our results in experimental myasthenia suggest that oral administration of AChR-specific recombinant fragments may be considered for antigen-specific immunotherapy of myasthenia gravis.

PubMedSearch : Im_1999_J.Clin.Invest_104_1723
PubMedID: 10606626

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Citations formats

Im SH, Barchan D, Fuchs S, Souroujon MC (1999)
Suppression of ongoing experimental myasthenia by oral treatment with an acetylcholine receptor recombinant fragment
J Clinical Investigation 104 :1723

Im SH, Barchan D, Fuchs S, Souroujon MC (1999)
J Clinical Investigation 104 :1723