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Updated: Aug 25, 2026
Myelin Oligodendrocyte Glycoprotein (MOG35-55) Induced Experimental Autoimmune Encephalomyelitis (EAE) in C57BL/6 Mice
Published on: April 15, 2014
A novel protective model against experimental allergic encephalomyelitis in mice expressing a transgenic TCR-specific
Itzhak Mendel1, Kannan Natarajan, Avraham Ben-Nun
1Laboratory of Immunology, Cellular Immunology Section, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11N315, 10 Center Drive, Bethesda, MD 20892-1892, USA.
Abstract:
Myelin oligodendrocyte glycoprotein (MOG) is an important autoantigen in multiple sclerosis and in experimental autoimmune encephalomyelitis (EAE). We generated a T cell receptor (TCR) transgenic (Tg) mouse expressing a TCR derived from an encephalitogenic T cell clone specific for MOG(35-55). This mouse failed to develop EAE spontaneously and developed mild EAE at late onset when immunized with MOG(35-55). The Tg T cells produced large amounts of IL-4 when stimulated with MOG(35-55) and underwent FAS/FAS-L-mediated activation-induced cell death when stimulated with MOG(35-55) and IL-12. The unique phenotype of these autoantigen-specific T cells may represent an important mechanism of protection against autoimmune disease.
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