Hoedemaekers A, Bessereau J L, Graus Y, Guyon T, Changeux J P, Berrih-Aknin S, van Breda Vriesman P, De Baets M H
Maastricht University, Department of Immunology, The Netherlands.
J Neuroimmunol. 1998 Aug 14;89(1-2):131-41. doi: 10.1016/s0165-5728(98)00126-x.
Injection of anti-AChR antibodies in passive transfer experimental autoimmune myasthenia gravis (EAMG) results in increased degradation of acetylcholine receptor (AChR) and increased synthesis of AChR alpha-subunit mRNA. Passive transfer of anti-Main Immunogenic Region (MIR) mAb 35 in aged rats does not induce clinical signs of disease nor AChR loss. The expression of the AChR subunit genes was analyzed in susceptible and resistant rats. In aged EAMG resistant rats, no increase in the amount of AChR alpha-subunit mRNA was measured. In vivo AChR degradation experiments did not show any increase in AChR degradation rates in aged resistant rats, in contrast to young susceptible rats. Taken together, these data demonstrate that resistance of the AChR protein to antibody-mediated degradation is the primary mechanism that accounts for the resistance to passive transfer EAMG in aged rats.
在被动转移实验性自身免疫性重症肌无力（EAMG）中注射抗乙酰胆碱受体（AChR）抗体，会导致乙酰胆碱受体（AChR）降解增加以及AChRα亚基mRNA合成增加。在老年大鼠中被动转移抗主要免疫原区（MIR）单克隆抗体35不会诱发疾病的临床症状，也不会导致AChR丢失。对易感和抗性大鼠的AChR亚基基因表达进行了分析。在老年EAMG抗性大鼠中，未检测到AChRα亚基mRNA量的增加。与年轻易感大鼠相反，体内AChR降解实验未显示老年抗性大鼠的AChR降解率有任何增加。综上所述，这些数据表明AChR蛋白对抗体介导的降解具有抗性是老年大鼠对被动转移EAMG产生抗性的主要机制。
