Pflugfelder C M, Cardinet G H, Lutz H, Holliday T A, Hansen R J
Muscle Nerve. 1981 Jul-Aug;4(4):289-95. doi: 10.1002/mus.880040405.
In the acquired form of myasthenia gravis in dogs, there are circulating antibodies to acetylcholine receptors (AChRs) and a reduction in the number of AChRs in the postsynaptic membrane. In this study, immune complexes were localized at the neuromuscular junctions in biopsy samples from 10 myasthenic dogs by immunocytochemical means employing conjugates of staphylococcal protein A and horseradish peroxidase. Immune complexes were observed in approximately 70% of the neuromuscular junctions studied in both type 1 and type 2 myofibers. Thus, acquired canine myasthenia gravis appears to involve immune-mediated mechanisms that destroy AChRs in a manner similar to myasthenia gravis in humans. Protein A was also observed to bind principally to elastic fibers in small arteries and arterioles of some myasthenic and control dogs; however, the significance of that localization is unknown.
在犬类获得性重症肌无力中,存在针对乙酰胆碱受体(AChRs)的循环抗体,且突触后膜中AChRs数量减少。在本研究中,通过使用葡萄球菌蛋白A与辣根过氧化物酶的结合物,采用免疫细胞化学方法,在10只患重症肌无力犬的活检样本神经肌肉接头处定位免疫复合物。在研究的1型和2型肌纤维中,约70%的神经肌肉接头处观察到免疫复合物。因此,获得性犬重症肌无力似乎涉及免疫介导机制,以与人类重症肌无力相似的方式破坏AChRs。在一些患重症肌无力犬和对照犬的小动脉和微动脉中,还观察到蛋白A主要与弹性纤维结合;然而,该定位的意义尚不清楚。