Dependency of Experimental Autoimmune Encephalomyelitis Induction on MOG(35-55) Properties Modulating Matrix Metalloproteinase-9 and Interleukin-6
- Authors
- Seo, Ji-Eun; Hasan, Mahbub; Han, Joon-Seung; Kim, Nak-Kyoon; Lee, Ji Eun; Lee, Kang Mi; Park, Ju-Hyung; Kim, Ho Jun; Son, Junghyun; Lee, Jaeick; Kwon, Oh-Seung
- Issue Date
- 2016-04
- Publisher
- SPRINGER/PLENUM PUBLISHERS
- Citation
- NEUROCHEMICAL RESEARCH, v.41, no.4, pp.666 - 676
- Abstract
- Experimental autoimmune encephalomyelitis (EAE) is commonly induced with myelin oligodendrocyte glycoprotein (MOG)(35-55); occasionally, EAE is not well induced despite MOG(35-55) immunization. To confirm that EAE induction varies with difference in MOG(35-55) properties, we compared three MOG(35-55) from different commercial sources, which are MOG-A, MOG-B, and MOG-C. The peptides induced EAE disease with 100, 40, and 20 % incidence, respectively. Compared with others, MOG-A showed higher peptide purity (99.2 %) and content (92.2 %) and presented a sheet shape with additional sodium and chloride chemical elements. In MOG-A-treated group, MMP-9 activity and IL-6 levels were considerably higher than the other groups in CNS tissues, and significantly increased VCAM-1, IFN-gamma, and decreased IL-4 were also shown compared to MOG-B- and/or MOG-C-treated group. In conclusion, the immunological and toxicological changes by the difference in MOG(35-55) properties modulate EAE induction, and MOG(35-55) which affects MMP-9 activity and IL-6 levels may be the most effective EAE-inducing antigen. This study can be potentially applied by researchers using MOG(35-55) peptide and manufacturers for MOG(35-55) synthesis.
- Keywords
- BLOOD-BRAIN-BARRIER; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; T-CELL RESPONSES; MULTIPLE-SCLEROSIS; ANIMAL-MODELS; MICE; EAE; AUTOANTIGEN; EXPRESSION; MIGRATION; MOG(35-55); EAE; MMP-9; IL-6; Property; Induction
- ISSN
- 0364-3190
- URI
- https://pubs.kist.re.kr/handle/201004/124239
- DOI
- 10.1007/s11064-015-1732-9
- Appears in Collections:
- KIST Article > 2016
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