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KMID : 0359320140540040209
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Korean Journal of Veterinary Research
2014 Volume.54 No. 4 p.209 ~ p.218
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Increased expression of galectin-9 in experimental autoimmune encephalomyelitis
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Cho Jin-Hee
Bing So-Jin
Kim A-Reum
Yu Hak-Sun
Lim Yoon-Kyu
Shin Tae-Kyun
Choi Jong-Hee
Jee Young-Heun
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Abstract
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Experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), reflects pathophysiologic steps in MS such as the influence of T cells and antibodies reactive to the myelin sheath, and the cytotoxic effect of cytokines. Galectin-9 (Gal-9) is a member of animal lectins that plays an essential role in various biological functions. The expression of Gal-9 is significantly enhanced in MS lesions; however, its role in autoimmune disease has not been fully elucidated. To identify the role of Gal-9 in EAE, we measured changes in mRNA and protein expression of Gal-9 as EAE progressed. Expression increased with disease progression, with a sharp rise occurring at its peak. Gal-9 immunoreactivity was mainly expressed in astrocytes and microglia of the central nervous system (CNS) and macrophages of spleen. Flow cytometric analysis revealed that Gal-9+CD11b+ cells were dramatically increased in the spleen at the peak of disease. Increased expression of tumor necrosis factor (TNF)-R1 and p-Jun Nterminal kinase (JNK) was observed in the CNS of EAE mice, suggesting that TNF-R1 and p-JNK might be key regulators contributing to the expression of Gal-9 during EAE. These results suggest that identification of the relationship between Gal-9 and EAE progression is critical for better understanding Gal-9 biology in autoimmune disease.
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KEYWORD
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central nervous system, experimental autoimmune encephalomyelitis, Galectin-9
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