The role of complement in experimental autoimmune myasthenia gravis
作者： Linda L. Kusner , Henry J. Kaminski
DOI: 10.1111/J.1749-6632.2012.06783.X
关键词: CD59 、 Immunology 、 Biology 、 Complement membrane attack complex 、 Myasthenia gravis 、 Complement system 、 Classical complement pathway 、 Decay-accelerating factor 、 Complement receptor 、 Complement component 3
摘要: Complement plays an important role in the pathophysiology of experimental autoimmune myasthenia gravis (EAMG). The deposition IgG at neuromuscular junction, followed by activation and observance C3 site, finally insertion membrane attack complex results destruction plasma junction. Animal models complement-deficient components show importance mediated lysis EAMG. These events have regulators that allow for limitation cascade ability cell to inhibit complement many places along pathway. regulatory proteins roles reducing inflammatory pathways. Mice deficient proteins, decay accelerating factor, CD59 demonstrate a significant increase Inhibition complement-mediated is attractive therapeutic MG.
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