Korean J Vet Res.  2014 Dec;54(4):209-218. 10.14405/kjvr.2014.54.4.209.

Increased expression of galectin-9 in experimental autoimmune encephalomyelitis

• Cho J
• Bing SJ
• Kim A
• Yu HS
• Lim YK
• Shin T
• Choi J
• Jee Y

• KMID: 2307885
• DOI: http://doi.org/10.14405/kjvr.2014.54.4.209

Abstract

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.

Keyword

central nervous system; experimental autoimmune encephalomyelitis; Galectin-9

MeSH Terms

Animals
Antibodies
Astrocytes
Autoimmune Diseases
Biology
Central Nervous System
Cytokines
Disease Progression
Encephalomyelitis, Autoimmune, Experimental*
Humans
Lectins
Macrophages
Mice
Microglia
Models, Animal
Multiple Sclerosis
Myelin Sheath
Phosphotransferases
RNA, Messenger
Spleen
T-Lymphocytes
Tumor Necrosis Factor-alpha
Antibodies
Cytokines
Lectins
Phosphotransferases
RNA, Messenger
Tumor Necrosis Factor-alpha