Role of the target organ in determining susceptibility to experimental autoimmune myasthenia gravis
Role of the target organ in determining susceptibility to experimental autoimmune myasthenia gravis
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DOI：
10.1016/s0165-5728(98)00126-x
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发表时间：
1998-08-14
影响因子：
3.3
通讯作者：
De Baets, MH
中科院分区：
文献类型：
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作者：
Hoedemaekers, A;Bessereau, JL;De Baets, MH
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）抗体导致乙酰胆碱受体（AChR）降解增加和AChR α亚基mRNA合成增加。在老年大鼠中被动转移抗主免疫原区（MIR） mAb 35不会诱导疾病的临床症状或AChR丢失。分析了acr亚基基因在易感和耐药大鼠中的表达情况。在老龄EAMG耐药大鼠中，AChR α亚基mRNA的数量未见增加。体内AChR降解实验显示，与年轻易感大鼠相比，老年耐药大鼠的AChR降解率没有增加。综上所述，这些数据表明，AChR蛋白抵抗抗体介导的降解是老年大鼠抵抗被动转移EAMG的主要机制。(C) 1998 Elsevier Science B.V.版权所有
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. (C) 1998 Elsevier Science B.V. All rights reserved.