J Neuroimmunol. 2004 Apr;149(1-2):10-21
Mendel I, Natarajan K, Ben-Nun A, Shevach EM.
Laboratory 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.
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.