In:
Journal of Virology, American Society for Microbiology, Vol. 72, No. 7 ( 1998-07), p. 6169-6174
Abstract:
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 (VP1 233–250 ), VP2 (VP2 74–86 ), and VP3 (VP3 24–37 ) 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.
Type of Medium:
Online Resource
ISSN:
0022-538X
,
1098-5514
DOI:
10.1128/JVI.72.7.6169-6174.1998
Language:
English
Publisher:
American Society for Microbiology
Publication Date:
1998
detail.hit.zdb_id:
1495529-5
