摘要
为探讨重症肌无力(MG)和实验性自身免疫性重症肌无力(EAMG)的发病机制,测定了小鼠抗人肌肉乙酰胆碱受体(AChR)单抗G10对健康大鼠的致病性以及G10可变区核苷酸序列。G10可使健康大鼠诱导出EAMG,其全身肌肉AChR损失率达28.8%±14.0%。G10的重链可变区(VH)基因由小鼠PC7183种系基因编码,与MOPC21VH种系基因的同源性为97.0%。G10的轻链可变区(VL)基因与抗DNA抗体的VL基因同源性为96.2%。从此结果可以看出,G10的重链(尤其是互补决定区3)在介导MG和EAMG中起更重要的作用。
Weinvestigatedthepathogenesisofmyastheniagravis(MG)ontheanimalmodelsofexperimentalautoimmunemyastheniagravis(EAMG).Thepathogenicityofamousemonoclonalan-tibody(G10)againsthumanmuscleacetylcholinereceptor(AChR)wasdeterminedontheratsandthenucleotideandaminoacidsequencesofvariableregionsofG10analyzed.G10passivelytrans-ferredintotheratswasabletoinduceEAMG,andAChRlossby28.8±14%.Theheavychainge-neticelementofG10,whichshoweda97.0%homologywithmostcloselyrelatedMOPC21germlineVH,wasderivedfromthemousePC7183germlinefamily.ThehomologyofvariableregionoflightchainbetweenG10andanti-DNAantibodywas96.2%.WewereoftheopinionthattheheavychainofmonoclonalantibodyagainstAChRplayedanimportantroleinmediatingMGandEAMG.
出处
《中华神经科杂志》
CAS
CSCD
1996年第5期283-285,共3页
Chinese Journal of Neurology