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Increased expression of galectin-9 in experimental autoimmune encephalomyelitis

실험적 자가면역성 뇌척수염을 유도한 마우스에서 Galectin-9의 과발현

  • Cho, Jinhee (Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University) ;
  • Bing, So Jin (Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University) ;
  • Kim, Areum (Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University) ;
  • Yu, Hak Sun (Department of Parasitology, School of Medicine, Pusan National University) ;
  • Lim, Yoon-Kyu (Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University) ;
  • Shin, Taekyun (Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University) ;
  • Choi, Jonghee (Department of Convergence Medical Science and Brain Korea 21 Plus Program, College of Oriental Medicine, Kyunghee University) ;
  • Jee, Youngheun (Department of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University)
  • 조진희 (제주대학교 수의과대학 수의학과) ;
  • 빙소진 (제주대학교 수의과대학 수의학과) ;
  • 김아름 (제주대학교 수의과대학 수의학과) ;
  • 유학선 (부산대학교 의학전문대학원 기생충학교실) ;
  • 임윤규 (제주대학교 수의과대학 수의학과) ;
  • 신태균 (제주대학교 수의과대학 수의학과) ;
  • 최종희 (경희대학교 한의과대학 융합과학교실) ;
  • 지영흔 (제주대학교 수의과대학 수의학과)
  • Received : 2014.02.03
  • Accepted : 2014.10.21
  • Published : 2014.12.31

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.

Keywords

References

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