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Specific removal of autoantibodies by extracorporeal immunoadsorption ameliorates experimental autoimmune myasthenia gravis
被引:11
作者:
Lazaridis, Konstantinos
[1
]
Dalianoudis, Ioannis
[2
]
Baltatzidi, Vasiliki
[1
]
Tzartos, Socrates J.
[1
,3
]
机构:
[1] Hellenic Pasteur Inst, 127 V Sofias Ave, GR-11521 Athens, Greece
[2] Thriassio Gen Hosp, Elefsina, Greece
[3] Univ Patra, Dept Pharm, Rion, Greece
关键词:
Myasthenia gravis;
Nicotinic acetylcholine receptor;
Immunoadsorption;
Therapy;
Experimental autoimmune myasthenia gravis;
NICOTINIC ACETYLCHOLINE-RECEPTOR;
MAIN IMMUNOGENIC REGION;
LOW-DENSITY-LIPOPROTEIN;
PATHOLOGICAL MECHANISMS;
EXTRACELLULAR DOMAINS;
MONOCLONAL-ANTIBODIES;
PASSIVE TRANSFER;
PLASMA-EXCHANGE;
EAMG MODEL;
RAT;
D O I:
10.1016/j.jneuroim.2017.09.001
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Myasthenia gravis (MG) is caused by autoantibodies, the majority of which target the muscle acetylcholine receptor (AChR). Plasmapheresis and IgG-immunoadsorption are useful therapy options, but are highly nonspecific. Antigen-specific immunoadsorption would remove only the pathogenic autoantibodies, reducing the possibility of side effects while maximizing the benefit. We have extensively characterized such adsorbents, but in vivo studies are missing. We used rats with experimental autoimmune MG to perform antigen-specific immunoadsorptions over three weeks, regularly monitoring symptoms and autoantibody titers. Immunoadsorption was effective, resulting in a marked autoantibody titer decrease while the immunoadsorbed, but not the mock treated, animals showed a dramatic symptom improvement. Overall, the procedure was found to be efficient, suggesting the subsequent initiation of clinical trials.
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页码:24 / 30
页数:7
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