Increased expression of galectin-9 in experimental autoimmune encephalomyelitis.
10.14405/kjvr.2014.54.4.209
- Author:
Jinhee CHO
1
;
So Jin BING
;
Areum KIM
;
Hak Sun YU
;
Yoon Kyu LIM
;
Taekyun SHIN
;
Jonghee CHOI
;
Youngheun JEE
Author Information
1. Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju 690-756, Korea. yhjee@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
central nervous system;
experimental autoimmune encephalomyelitis;
Galectin-9
- MeSH:
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
- From:Korean Journal of Veterinary Research
2014;54(4):209-218
- CountryRepublic of Korea
- Language:Korean
-
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.
