| Increased expression of galectin-9 in experimental autoimmune encephalomyelitis |
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Jinhee Cho1, So Jin Bing1, Areum Kim1, Hak Sun Yu2, Yoon-Kyu Lim1, Taekyun Shin1, Jonghee Choi3, Youngheun Jee1 |
1Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University
2Department of Parasitology, School of Medicine, Pusan National University
3Department of Convergence Medical Science and Brain Korea 21 Plus Program, College of Oriental Medicine, Kyunghee University |
| 실험적 자가면역성 뇌척수염을 유도한 마우스에서 Galectin-9의 과발현 |
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조진희1, 빙소진1, 김아름1, 유학선2, 임윤규1, 신태균1, 최종희3, 지영흔1 |
1제주대학교 수의과대학 수의학과
2부산대학교 의학전문대학원 기생충학교실
3경희대학교 한의과대학 융합과학교실 |
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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 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. |
| Key Words:
central nervous system, experimental autoimmune encephalomyelitis, Galectin-9 |
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