EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS - CELLULAR AND HUMORAL IMMUNE-RESPONSES
EXPERIMENTAL AUTOIMMUNE MYASTHENIA-GRAVIS - CELLULAR AND HUMORAL IMMUNE-RESPONSES
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DOI：
10.1111/j.1749-6632.1976.tb47693.x
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发表时间：
1976-01-01
影响因子：
5.2
通讯作者：
SEYBOLD, ME
中科院分区：
文献类型：
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作者：
LENNON, VA;LINDSTROM, JM;SEYBOLD, ME
皮内接种鳗鱼乙酰胆碱受体蛋白（AChR）与佐剂的大鼠产生骨骼肌AChR的自身免疫。这在临床上被证明为实验性自身免疫性重症肌无力（EAMG）的两次发作，急性期发生在早期（8天）并且是短暂的，而慢性期（30天）通常是进行性的。阳性延迟皮肤反应出现在第4天和血清抗体鳗鱼AChR检测到接种后7天。第25天后，抗同基因肌AChR抗体滴度急剧上升。抗肌肉AChR抗体呈7S沉淀。AChR致敏大鼠淋巴结细胞可将EAMG转移至正常受体。EAMG发作后行胸腺切除术无效。体内早期抗胸腺细胞血清治疗可抑制急性期EAMG，但不抑制慢性期EAMG。结合胸腺切除、X射线照射和不同淋巴细胞群的重建的实验表明，胸腺来源的淋巴细胞是诱导EAMG和AChR抗体所必需的。这些数据表明，细胞和体液的AChR反应，无论是顺序或组合，有助于EAMG的发病机制。
Rats inoculated intradermally with eel acetylcholine receptor protein (AChR) with adjuvants developed autoimmunity to skeletal muscle AChR. This is evidenced clinically as two episodes of experimental autoimmune myasthenia gravis (EAMG), an acute phase that occurs early (8 days) and is transient, and a chronic phase (30 days) that is usually progressive. Positive delayed cutaneous reactivity appeared at day 4 and serum antibody to eel AChR was detectable by day 7 postinoculation. After day 25 the titer of antibody to syngeneic muscle AChR rose abruptly. Antibody to muscle AChR sedimented as 7S. Lymph node cells from rats sensitized to AChR were capable of transferring EAMG to normal recipients. Thymectomy after the onset of EAMG had no effect. Early treatment in vivo with antithymocyte serum suppressed acute but not chronic phase EAMG. Experiments combining thymectomy, x-irradiation and reconstitution with distinct populations of lymphocytes indicated athat thymus-derived lymphocytes are required for induction of EAMG and antibody to AChR. These data suggest that both cellular and humoral responses to AChR, either sequentially or in combination, contribute to the pathogenesis of EAMG.