TY - JOUR
T1 - Immunosuppression of rat myasthenia gravis by oral administration of a syngeneic acetylcholine receptor fragment
AU - Maiti, Prasanta K.
AU - Feferman, Tali
AU - Im, Sin Hyeog
AU - Souroujon, Miriam C.
AU - Fuchs, Sara
N1 - Funding Information:
This work was supported by grants from The Muscular Dystrophy Association of America (MDA), The Association Francaise Contre les Myopathies (AFM), The European Commission (EC, No QLG1-CT-2001-10918 and QLRT-2001-00225), The Abramson Family Foundation and The Wood-Byer Foundation.
PY - 2004/7
Y1 - 2004/7
N2 - A syngeneic rat recombinant fragment of the extracellular domain of the acetylcholine receptor (AChR) α-subunit (Rα1-205), 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-γ and TNF-α, upregulated IL-10, changes in anti-AChR IgG isotypes and diminished Th1 signaling via CD28/CTLA-4:B7. Unlike the xenogeneic fragment, the syngeneic Rα1-205 does not induce elevation in TGF-β 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.
AB - A syngeneic rat recombinant fragment of the extracellular domain of the acetylcholine receptor (AChR) α-subunit (Rα1-205), 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-γ and TNF-α, upregulated IL-10, changes in anti-AChR IgG isotypes and diminished Th1 signaling via CD28/CTLA-4:B7. Unlike the xenogeneic fragment, the syngeneic Rα1-205 does not induce elevation in TGF-β 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.
KW - Autoimmunity
KW - Mucosal tolerance
KW - Myasthenia gravis
KW - Th1/Th2 cells
UR - http://www.scopus.com/inward/record.url?scp=3042656879&partnerID=8YFLogxK
U2 - 10.1016/j.jneuroim.2004.04.010
DO - 10.1016/j.jneuroim.2004.04.010
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C2 - 15223243
AN - SCOPUS:3042656879
SN - 0165-5728
VL - 152
SP - 112
EP - 120
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -