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Title: Immunosuppression of rat myasthenia gravis by oral administration of a syngeneic acetylcholine receptor fragment. Author: Maiti PK, Feferman T, Im SH, Souroujon MC, Fuchs S. Journal: J Neuroimmunol; 2004 Jul; 152(1-2):112-20. PubMed ID: 15223243. Abstract: A syngeneic rat recombinant fragment of the extracellular domain of the acetylcholine receptor (AChR) alpha-subunit (Ralpha1-205), administered orally, suppresses ongoing experimental autoimmune myasthenia gravis (EAMG) in rats. The underlying mechanism is a shift from Th1 to Th2 regulation as evidenced by downregulated mRNA expression levels of IFN-gamma and TNF-alpha, upregulated IL-10, changes in anti-AChR IgG isotypes and diminished Th1 signaling via CD28/CTLA-4:B7. Unlike the xenogeneic fragment, the syngeneic Ralpha1-205 does not induce elevation in TGF-beta and elicitation of autoregulatory cells. The ability to suppress EAMG by a non-immunogenic syngeneic fragment of AChR is encouraging and may in the future be applied for the treatment of myasthenia gravis in humans.[Abstract] [Full Text] [Related] [New Search]