Exacerbation of experimental autoimmune encephalomyelitis by passive transfer of IgG antibodies from a multiple sclerosis patient responsive to immunoadsorption

被引:11
|
作者
Pedotti, Rosetta [1 ]
Musio, Silvia [1 ]
Scabeni, Stefano [1 ]
Farina, Cinthia [1 ,2 ]
Poliani, Pietro Luigi [3 ]
Colombo, Emanuela [2 ]
Costanza, Massimo [1 ]
Berzi, Angela [1 ]
Castellucci, Fabrizio [4 ]
Ciusani, Emilio [5 ]
Confalonieri, Paolo [1 ]
Hemmer, Bernhard [6 ]
Mantegazza, Renato [1 ]
Antozzi, Carlo [1 ]
机构
[1] Fdn IRCCS Neurol Inst C Besta, Neuroimmunol & Neuromuscular Disorders Unit, I-20133 Milan, Italy
[2] Ist Sci San Raffaele, Inst Expt Neurol INSpe, I-20132 Milan, Italy
[3] Univ Brescia, Dept Pathol, I-25123 Brescia, Italy
[4] Bocconi Univ, Dept Management & Technol, I-20136 Milan, Italy
[5] Fdn IRCCS Neurol Inst C Besta, Lab Clin Pathol & Med Genet, I-20133 Milan, Italy
[6] Univ Dusseldorf, Dept Neurol, D-40225 Dusseldorf, Germany
关键词
Multiple sclerosis; Experimental autoimmune encephalomyelitis; Antibodies; Demyelination; Plasma exchange; Immunoadsorption; CENTRAL-NERVOUS-SYSTEM; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; PLASMA-EXCHANGE; DEMYELINATION; DISEASE; AUTOANTIBODIES; LESIONS; MOUSE; IDENTIFICATION; DECARBOXYLASE;
D O I
10.1016/j.jneuroim.2013.05.010
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The pathogenic role of antibodies in multiple sclerosis (MS) is still controversial. We transferred to mice with experimental autoimmune encephalomyelitis (EAE), animal model of MS, IgG antibodies purified from a MS patient presenting a dramatic clinical improvement during relapse after selective IgG removal with immunoadsorption. Passive transfer of patient's IgG exacerbated motor paralysis and increased mouse central nervous system (CNS) inflammation and demyelination. Binding of patient's IgG was demonstrated in mouse CNS, with a diffuse staining of white matter oligodendrocytes. These data support a growing body of evidence that antibodies can play an important role in the pathobiology of MS. (C) 2013 Elsevier B.V. All rights reserved.
引用
收藏
页码:19 / 26
页数:8
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