ANTIGENIC MODULATION AND RECEPTOR LOSS IN EXPERIMENTAL AUTO-IMMUNE MYASTHENIA-GRAVIS
ANTIGENIC MODULATION AND RECEPTOR LOSS IN EXPERIMENTAL AUTO-IMMUNE MYASTHENIA-GRAVIS
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DOI：
10.1002/mus.880020304
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发表时间：
1979-01-01
期刊：
影响因子：
3.4
通讯作者：
EINARSON, B
中科院分区：
文献类型：
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作者：
LINDSTROM, J;EINARSON, B
用0.1-100 μ g从Torpedo californica的电器官纯化的乙酰胆碱受体（AChR）免疫大鼠组，导致剂量依赖性的：大鼠肌肉中的ACR损失;抗体与保留在肌肉中的许多受体结合;以及在血清中产生能够与从大鼠肌肉溶解的受体交叉反应的抗体。此外，从大鼠免疫的电器官乙酰胆碱受体的肌肉细胞培养引起的受体的损失，加速受体的降解速率。单价抗体片段不加速降解，除非加入抗抗体以交联与受体结合的单价抗体片段。显然，通过抗体分子交联受体会引发加速的受体降解，导致受体丢失。由于体外观察到的抗原调节，受体破坏率增加似乎足以解释体内观察到的受体损失程度。抗体交联受体内吞作用可能是体外和体内抗原调节的共同限速步骤。
Immunization of groups of rats with 0.1-100 .mu.g of acetylcholine receptor (AChR) purified from the electric organ of Torpedo californica resulted in dose-dependent: ACR loss from the rats'' muscles; antibody binding to many of the receptors remaining in muscle; and production of antibodies in serum capable of cross-reacting with receptor solubilized from rat muscle. Addition of antibodies from rats immunized with electric organ acetylcholine receptors to muscle cells in culture caused loss of receptor by accelerating the receptor degradation rate. Monovalent antibody fragments did not accelerate degradation unless antiantibody was added to cross-link the monovalent antibody fragments bound to receptors. Apparently cross-linking of receptors by antibody molecules triggers accelerated receptor degradation, leading to receptor loss. The rate of receptor destruction increase due to antigenic modulation observed in vitro appears sufficient to account for the extent of receptor loss observed in vivo. Antibody cross-linked receptor endocytosis may be a rate-limiting step common to antigenic modulation in vitro and in vivo.