Myasthenia gravis (MG) and its animal model experimental autoimmune myasthenia gravis (EAMG)
are caused by autoantibodies against nicotinic acetylcholine receptor (AChR)
重症肌無力(MG)及其動物模型實驗性自身免疫性重症肌無力(EAMG)是由骨骼肌中菸鹼型乙醯膽鹼受體(AChR)的自身抗體引起的。
Emerging investigations of the roles of cytokines in MG and EAMG
have revealed that the Th2 cell related cytokine interleukin 4 (IL-4),
an efficient growth promoter for B-cell proliferation and differentiation,
is important for anti-AChR antibody production.
Th2細胞相關的細胞因子白細胞介素4(IL-4),對 抗AChR抗體 的產生很重要。
IL-6 and IL-10 have similar effects.
IL-10具有相似的作用。
These clones helped production of antibody to AChR by B cells which was found to be regulated primarily by IL-4, not by IL-2, secreted by the T cells in response to AChR.
B細胞產生針對AChR的抗體,其被發現主要由IL-4調節,而不是由響應於AChR的T細胞分泌的IL-2調節。
Abnormal sympathetic hyper-reactivity in patients with myasthenia gravis
重症肌無力患者的交感神經過度反應異常