Increased expression of galectin-9 in experimental autoimmune encephalomyelitis
2014
Cho, J.H., Jeju National University, Jeju, Republic of Korea | Bing, S.J., Jeju National University, Jeju, Republic of Korea | Kim, A.R., Jeju National University, Jeju, Republic of Korea | Yu, H.S., Pusan national University, Yangsan, Republic of Korea | Lim, Y.K., Jeju National University, Jeju, Republic of Korea | Shin, T.Y., Jeju National University, Jeju, Republic of Korea | Choi, J.H., Kyunghee University, Seoul, Republic of Korea | Jee, Y.H., Jeju National University, Jeju, Republic of Korea
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 N-terminal 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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