Glycobiology Advance Access originally published online on February 26, 2008
Glycobiology 2008 18(5):408-413; doi:10.1093/glycob/cwn017
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Roles of complex gangliosides in the development of experimental autoimmune encephalomyelitis
2 Department of Neurology, Kinki University School of Medicine, Osaka
3 Department of Biochemistry, Nagoya University School of Medicine, Nagoya, Japan
1 To whom correspondence should be addressed: Tel: +81-72-366-0221; Fax: +81-72-368-4846; e-mail: kusunoki-tky{at}umin.ac.jp
Received on September 11, 2007; revised on December 28, 2007; accepted on February 20, 2008
We induced experimental autoimmune encephalomyelitis (EAE) in GM2/GD2 synthase knockout mice (GM2/GD2–/–), which cannot synthesize complex gangliosides, such as GM1, GD1a, GD1b, GT1b, and GQ1b, to investigate the roles of complex gangliosides in the pathogenesis of this disease. We used myelin-oligodendrocyte glycoprotein (MOG) as an immunogen. In active immunization EAE, the severity of clinical score was not different but the disease onset was significantly delayed in GM2/GD2–/– compared with those in wild-type mice. When we transferred MOG-reactive T cells from GM2/GD2–/– or wild-type mice to wild-type mice, no significant differences were observed between the two groups. In contrast, when we transferred MOG-reactive T cells from wild-type mice to GM2/GD2–/– or to wild-type mice, the onset of EAE in GM2/GD2–/– mice was delayed. The recall response of MOG-specific T cells, the function of antigen presenting cells, or the expression of several adhesion molecules in the endothelium were not significantly different between GM2/GD2–/– and wild-type mice. On the other hand, quantitative analysis of cellular infiltration in the central nervous system (CNS) on day 9 of active immunization EAE showed that the CD4+ cell number in the CNS isolated from GM2/GD2–/– mice was significantly less than that from wild-type mice. It indicated that the delayed onset of EAE in GM2/GD2–/– mice was due to the delay of the migration of pathogenic T cells into the CNS. Thus, the complex gangliosides may be involved in the T cell–endothelial cell interaction in the pathogenetic process of EAE.
Key words: EAE / MS / neuroimmunology / rodent / cell surface molecules
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J. Wang, Z.-H. Lu, H.-J. Gabius, C. Rohowsky-Kochan, R. W. Ledeen, and G. Wu Cross-Linking of GM1 Ganglioside by Galectin-1 Mediates Regulatory T Cell Activity Involving TRPC5 Channel Activation: Possible Role in Suppressing Experimental Autoimmune Encephalomyelitis J. Immunol., April 1, 2009; 182(7): 4036 - 4045. [Abstract] [Full Text] [PDF]
|
|