The Journal of Experimental Medicine
Janeway's Immunobiology 7th Edition
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Published 5 May 2003. doi:10.1084/jem.20021603
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© Rockefeller University Press, 0022-1007/2003/5/1073 $5.00
The Journal of Experimental Medicine, Volume 197, Number 9, 1073-1081

Myelin Oligodendrocyte Glycoprotein–specific T Cell Receptor Transgenic Mice Develop Spontaneous Autoimmune Optic Neuritis

Estelle Bettelli1, Maria Pagany2, Howard L. Weiner1, Christopher Linington2,3, Raymond A. Sobel4,5 and Vijay K. Kuchroo1

1 Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115
2 Department of Neuroimmunology, Max-Planck Institute for Neuroimmunology, 82152 Martinsried, Germany
3 Department of Medicine and Therapeutics, Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, United Kingdom
4 Laboratory Service, Veterans Affairs Health Care System, Palo Alto, CA 94304
5 Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305

Address correspondence to Vijay K. Kuchroo, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115. Phone: 617-525-5350; Fax: 617-525-5333; E-mail: vkuchroo{at}rics.bwh.harvard.edu

Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system (CNS) that in many patients first presents clinically as optic neuritis. The relationship of optic neuritis to MS is not well understood. We have generated novel T cell receptor (TCR) transgenic mice specific for myelin oligodendrocyte glycoprotein (MOG). MOG-specific transgenic T cells are not deleted nor tolerized and are functionally competent. A large proportion (>30%) of MOG-specific TCR transgenic mice spontaneously develop isolated optic neuritis without any clinical nor histological evidence of experimental autoimmune encephalomyelitis (EAE). Optic neuritis without EAE could also be induced in these mice by sensitization with suboptimal doses of MOG. The predilection of these mice to develop optic neuritis is associated with higher expression of MOG in the optic nerve than in the spinal cord. These results demonstrate that clinical manifestations of CNS autoimmune disease will vary depending on the identity of the target autoantigen and that MOG-specific T cell responses are involved in the genesis of isolated optic neuritis.

Key Words: MOG • experimental autoimmune encephalomyelitis • multiple sclerosis • autoimmunity of CNS • disease model


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