Protracted, relapsing and demyelinating experimental autoimmune encephalomyelitis in DA rats immunized with syngeneic spinal cord and incomplete Freund's adjuvant

被引:118
作者
Lorentzen, JC
Issazadeh, S
Storch, M
Mustafa, MI
Lassman, H
Linington, C
Klareskog, L
Olsson, T
机构
[1] KAROLINSKA INST,KAROLINSKA HOSP,MOLEC MED UNIT,S-17176 STOCKHOLM,SWEDEN
[2] KAROLINSKA INST,KAROLINSKA HOSP,DEPT NEUROL,S-17176 STOCKHOLM,SWEDEN
[3] MAX PLANCK INST PSYCHIAT,DEPT NEUROIMMUNOL,W-8033 MARTINSRIED,GERMANY
[4] UNIV VIENNA,NEUROL INST,A-1090 VIENNA,AUSTRIA
关键词
central nervous system; myelin basic protein; T cells; multiple sclerosis;
D O I
10.1016/0165-5728(95)00153-0
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis (MS). However, MS is a chronic, relapsing and demyelinating disease, whereas EAE in rats is typically a brief and monophasic disorder showing little demyelination. We demonstrate here that DA rats develop severe, protracted and relapsing EAE (SPR-EAE) after a subcutaneous immunization at the tail base with syngeneic spinal cord and incomplete Freund's adjuvant (IFA). The neurological deficits were accompanied by demyelinating inflammatory lesions in the spinal cord, with infiltrating T lymphocytes and perivascular deposition of immunoglobulins and complement. The induction of SPR-EAE was associated with humoral autoreactivity to myelin oligodendrocyte glycoprotein (MOG) and cellular autoreactivity to the rat myelin basic protein (MBP) peptides 69-87 and 87-101. These two peptides, as well as whole rat MBP, were encephalitogenic. In conclusion, we believe that the presently described demyelinating SPR-EAE represents a useful model for MS.
引用
收藏
页码:193 / 205
页数:13
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