Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 197, Issue 9, Pages 1073-1081Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20021603
Keywords
MOG; experimental autoimmune encephalomyelitis; multiple sclerosis; autoimmunity of CNS; disease model
Categories
Funding
- Multiple Sclerosis Society [560] Funding Source: Medline
- NINDS NIH HHS [R01 NS 38037, R01 NS035685, R01 NS 35685, R01 NS 30843, P01 NS038037, R01 NS030843] Funding Source: Medline
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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.
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