期刊
NEURAL REGENERATION RESEARCH
卷 8, 期 35, 页码 3296-3305出版社
SHENYANG EDITORIAL DEPT NEURAL REGENERATION RES
DOI: 10.3969/j.issn.1673-5374.2013.35.004
关键词
neural regeneration; experimental allergic encephalomyelitis; multiple sclerosis; animal models; autoimmune disease; costimulatory signal; costimulatory molecule; programmed cell death 1 ligand 1; B7-CD28 superfamily; grants-supported paper; neuroregeneration
资金
- Natural Science Foundation of Jiangsu Province in China [BK2011267]
Experimental allergic encephalomyelitis is a mouse model of human multiple sclerosis with similar pathology and pathogenesis. Th1 cells play an important role in the pathogenesis of experimental allergic encephalomyelitis. This study determined the potential effect of programmed cell death 1 ligand 1 in the pathogenesis of experimental allergic encephalomyelitis induced by injecting myelin oligodendrocyte glycoprotein, complete Freund's adjuvant and Bordetella pertussis toxin into C57BL/6J mice. Experimental allergic encephalomyelitis mice developed disease and showed inflammatory changes in the central nervous system by hematoxylin-eosin staining of spinal cord pathological sections, demyelination by Luxol fast-blue staining and clinical manifestations. The expression of programmed cell death 1 ligand 1 in mice was detected by immunohistochemistry, flow cytometry and western blot analysis. The expression of programmed cell death 1 ligand 1 in the spinal cord and splenocytes of mice was significantly increased compared with normal mice. Our findings suggest the involvement of programmed cell death 1 ligand 1 in the pathogenesis of experimental allergic encephalomyelitis and suggest this should be studied in multiple sclerosis.
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