ملخص
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.
اللغة الأصلية | الإنجليزيّة |
---|---|
الصفحات (من إلى) | 112-120 |
عدد الصفحات | 9 |
دورية | Journal of Neuroimmunology |
مستوى الصوت | 152 |
رقم الإصدار | 1-2 |
المعرِّفات الرقمية للأشياء | |
حالة النشر | نُشِر - يوليو 2004 |
ملاحظة ببليوغرافية
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.