实验性自身免疫性重症肌无力：细胞免疫和体液免疫反应

Experimental autoimmune myasthenia gravis: cellular and humoral immune responses.

作者信息

Lennon V A, Lindstrom J M, Seybold M E

出版信息

Ann N Y Acad Sci. 1976;274:283-99. doi: 10.1111/j.1749-6632.1976.tb47693.x.

DOI:10.1111/j.1749-6632.1976.tb47693.x

Abstract

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.

摘要

用鳗鲡乙酰胆碱受体蛋白（AChR）与佐剂进行皮内接种的大鼠，会产生针对骨骼肌AChR的自身免疫。这在临床上表现为实验性自身免疫性重症肌无力（EAMG）的两个阶段，一个是早期（8天）出现的急性期，为短暂性，另一个是慢性期（30天），通常呈进行性发展。在接种后第4天出现阳性迟发性皮肤反应，接种后第7天可检测到抗鳗鲡AChR的血清抗体。25天后，同基因肌肉AChR的抗体效价突然升高。肌肉AChR抗体以7S形式沉淀。对AChR致敏的大鼠的淋巴结细胞能够将EAMG转移给正常受体。EAMG发病后进行胸腺切除术无效。在体内用抗胸腺细胞血清进行早期治疗可抑制急性期而非慢性期的EAMG。将胸腺切除术、X射线照射和用不同淋巴细胞群体进行重建的实验表明，胸腺来源的淋巴细胞是诱导EAMG和抗AChR抗体所必需的。这些数据表明，对AChR的细胞和体液反应，无论是顺序发生还是同时发生，都对EAMG的发病机制有影响。