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J Virol, July 1998, p. 6169-6174, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Role of Individual T-Cell Epitopes of Theiler's Virus in the Pathogenesis of Demyelination Correlates with the Ability To Induce a Th1 Response

Robert L. Yauch,1,dagger JoAnn P. Palma,1 Hiroyuki Yahikozawa,1,2 Chang-Sung Koh,2 and Byung S. Kim1,*

Departments of Microbiology-Immunology and Pathology, Northwestern University Medical School, Chicago, Illinois 60611,1 and Department of Medicine (Neurology), Shinshu University Medical School, Matsumoto 390, Japan2

Received 20 January 1998/Accepted 2 April 1998

Intracerebral inoculation of susceptible strains of mice with Theiler's murine encephalomyelitis virus (TMEV) results in immune-mediated demyelination. Three major T-cell epitopes have previously been identified within the VP1 (VP1233-250), VP2 (VP274-86), and VP3 (VP324-37) capsid proteins in virus-infected SJL/J mice. These epitopes appear to account for the majority (~90%) of major histocompatibility complex class II-restricted T-cell responses to TMEV. Interestingly, the effect of immunization with synthetic peptides bearing the predominant T-cell epitopes on the course of TMEV-induced demyelination indicates that T cells reactive to the VP1 and VP2 epitopes, but not VP3, accelerate the pathogenesis of demyelination. The predominant pathogenic role of the T cells is verified by similar immunization with the fusion proteins containing the entire individual capsid proteins. The order of appearance and level of T cells specific for the individual epitopes during the course of demyelination are similar to each other. However, cytokine profiles of T cells from virus-infected mice indicate that T cells specific for the VP1 (and perhaps the VP2) epitope are Th1, whereas T cells reactive to VP3 are primarily Th2. These results suggest that Th1-type cells specific for VP1 and VP2 are involved in the pathogenesis of viral demyelination induced by TMEV. Thus, a predominance of Th1-inducing viral epitopes is likely critical for the pathogenesis of demyelination.

* Corresponding author. Mailing address: Department of Microbiology-Immunology, Northwestern University Medical School, 303 East Chicago Ave., Chicago, IL 60611. Phone: (312) 503-8693. Fax: (312) 503-1339. E-mail: bskim{at}nwu.edu.

dagger Present address: Division of Tumor Virology, Dana-Farber Cancer Center, Boston, MA 02115.

J Virol, July 1998, p. 6169-6174, Vol. 72, No. 7
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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