期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 210, 期 1-2, 页码 13-21出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2009.02.013
关键词
Cuprizone; Demyelination; EAE; Tolerance; MOG; MS
资金
- MS Australia
- The National Health and Medical Research Council of Australia
Myelin reactive T cells are central in the development of the autoimmune response leading to CNS destruction in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis (EAE). Investigations on the mechanisms underlying the activation and expansion of myelin reactive T have stressed the importance of non-autoimmune conditions impinging the autoimmune repertoire potentially involved in the disease. Here, we show that CNS injury caused by the toxic cuprizone results in the generation of immunoreactivity towards several myelin components. Paradoxically, exposure to CNS injury does not increase the susceptibility to develop EAE, but render mice protected to the pathogenic autoimmune response against myelin antigens. (C) 2009 Elsevier B.V. All rights reserved.
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