PD-L1 is increased in the spinal cord and infiltrating lymphocytes in experimental allergic encephalomyelitis

Experimental allergic encephalomyelitis is a mouse model of human multiple sclerosis with similar pathology and pathogenesis. Thl cells play an important role in the pathogenesis of experimental allergic encephalomyelitis. This study determined the potential effect of programmed cell death 1 ligand...

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Published inNeural regeneration research Vol. 8; no. 35; pp. 3296 - 3305
Main Authors Li, Min, Jiang, Jiandong, Fu, Bing, Chen, Jiechun, Xue, Qun, Dong, Wanli, Gu, Yanzheng, Tang, Lingtao, Xue, Limin, Fang, Qi, Wang, Mingyuan, Zhang, Xueguang
Format Journal Article
LanguageEnglish
Published India Medknow Publications and Media Pvt. Ltd 15.12.2013
Department of Neurology, Second People’s Hospital of Lianyungang City, Lianyungang 222006, Jiangsu Province, China%Department of Neurology, First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China%Institute of Clinical Immunology, Soochow University, Suzhou 215006, Jiangsu Province, China%Department of Neurology, Third Hospital of Xingtai City, Xingtai 054000, Hebei Province, China%Red-Cross Blood Center of Suzhou City, Suzhou 215006, Jiangsu Province, China
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Summary:Experimental allergic encephalomyelitis is a mouse model of human multiple sclerosis with similar pathology and pathogenesis. Thl 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 in- flammatory 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 anatysis. 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 ex- perimental allergic encephalomyelitis and suggest this should be studied in multiple sclerosis.
Bibliography:Experimental allergic encephalomyelitis is a mouse model of human multiple sclerosis with similar pathology and pathogenesis. Thl 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 in- flammatory 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 anatysis. 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 ex- perimental allergic encephalomyelitis and suggest this should be studied in multiple sclerosis.
neural regeneration; experimental allergic encephalomyelitis; multiple sclerosisautoimmune disease; costimulatory signal; costimulatory molecule; programmed ce1; B7-CD28 superfamily; grants-supported paper; neuroregenerationanimal models;II death 1 ligand
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Author statements: The manuscript is original, has not been submitted to or is not under consideration by another publication, has not been previously published in any language or any form, including electronic, and contains no disclosure of confidential information or authorship/patent application/funding source disputations.
Author contributions: Xue Q, Dong WL, and Jiang JD designed the experiments. Li M, Fu B, Gu YZ, Tang LT, and Xue LM implemented the experiments. Zhang XG, Fang Q, and Wang MY assessed the experiments. Li M and Fu B collected data. Xue Q and Li M drafted the manuscript. Zhang XG, Xue Q, and Dong WL revised the manuscript. Dong WL, Xue Q, and Li M were responsible for the article. All authors approved the final version of the manuscript.
Min Li and Jiandong Jiang contributed equally to this work.
Min Li, Master, Attending physician.
ISSN:1673-5374
1876-7958
DOI:10.3969/j.issn.1673-5374.2013.35.004