Author: Cirone, Mara; Cuomo, Laura; Zompetta, Claudia; Ruggieri, Stefano; Frati, Luigi; Faggioni, Alberto; Ragona, Giuseppe
Title: Human herpesvirus 6 and multiple sclerosis: A study of t cell crossâ€reactivity to viral and myelin basic protein antigens Cord-id: um4pqkuo Document date: 2002_8_12
ID: um4pqkuo
Snippet: Several reports have suggested an association of human herpesvirus 6 (HHVâ€6) with multiple sclerosis. Autoreactive T lymphocytes directed against myelin components seem to contribute to the pathogenesis of the disease. It has been suggested that molecular mimicry between viral and selfâ€antigens might be one of the mechanisms that determine the onset of several autoimmune diseases. Following this hypothesis, the purpose of the present study was to evaluate if HHVâ€6 could play a role in acti
Document: Several reports have suggested an association of human herpesvirus 6 (HHVâ€6) with multiple sclerosis. Autoreactive T lymphocytes directed against myelin components seem to contribute to the pathogenesis of the disease. It has been suggested that molecular mimicry between viral and selfâ€antigens might be one of the mechanisms that determine the onset of several autoimmune diseases. Following this hypothesis, the purpose of the present study was to evaluate if HHVâ€6 could play a role in activating T cells capable of crossâ€reaction with an important myelin component, the myelin basic protein. T cell lines were established from 22 multiple sclerosis patients and from 16 healthy controls, and their capability to react to both virus and myelin basic protein antigens was compared. The analysis of T cell crossâ€reactivity in patients and controls did not show significant differences in the HHVâ€6 ability to activate myelin basic proteinâ€reactive T cells. Similarly, the evaluation of the humoral immune response to HHVâ€6 in patients and controls did not mirror any abnormality in the HHVâ€6 status in multiple sclerosis patients. Therefore, although the findings of activity in vitro of T cell lines with dual specificity are consistent with the hypothesis of molecular mimicry, the lack of differences in crossâ€reactivity between patients and controls do not support molecular mimicry as an important mechanism in the physiopathology of this disease. J. Med. Virol. 68: 268–272, 2002. © 2002 Wileyâ€Liss, Inc.
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