Pachner A R, Kantor F S
Clin Exp Immunol. 1984 Jun;56(3):659-68.
Immunization of C57Bl/6 mice with Torpedo acetylcholine receptor (AChR) leads to EAMG, experimental autoimmune myasthenia gravis, with characteristic clinical, electrophysiological, and immune features. Present in the lymphoid organs of mice with EAMG are AChR specific suppressor T cells: these cells can be grown in vitro as T cell lines. These lines are able to suppress the in vitro response to AChR, and can suppress the in vivo development of EAMG.
用鱼雷乙酰胆碱受体(AChR)免疫C57Bl/6小鼠会导致实验性自身免疫性重症肌无力(EAMG),其具有典型的临床、电生理和免疫特征。EAMG小鼠的淋巴器官中存在AChR特异性抑制性T细胞:这些细胞可在体外培养成T细胞系。这些细胞系能够抑制体外对AChR的反应,并能抑制EAMG在体内的发展。