Cell-mediated autoimmunity has been strongly implicated in the pathogenesis of the myocardial cell damage involved in viral myocarditis. Using a murine model of acute myocarditis caused by Coxsackievirus B3 (CVB3), perforin-expressing killer cells have been shown to infiltrate the heart, and interce
RESTRICTED USAGE OF T-CELL RECEPTOR Vα GENES IN INFILTRATING CELLS IN MURINE HEARTS WITH ACUTE MYOCARDITIS CAUSED BY COXSACKIE VIRUS B3
✍ Scribed by SEKO, YOSHINORI; YOSHIFUMI, ENOKAWA; YAGITA, HIDEO; OKUMURA, KO; YAZAKI, YOSHIO
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 493 KB
- Volume
- 178
- Category
- Article
- ISSN
- 0022-3417
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✦ Synopsis
In murine myocarditis, it has been shown that natural killer cells first infiltrate the heart, followed by activated T-cells, which play an important role in the pathogenesis of the myocardial damage. In the same model of acute myocarditis, the repertoire of T-cell receptor (TCR) V p genes in infiltrating cells in the heart has also been shown to be restricted. To study the nature of T-cell infiltration in more detail, the expression of TCR V a genes in infiltrating cells in the heart has been analysed by the polymerase chain reaction (PCR), confirmed by Southern blot hybridization with a Ca cDNA probe. In contrast to spleen lymphocytes, the repertoire of Va gene transcripts in the heart was restricted. Infiltrating cells expressing Val0 were found in five of eight hearts of mice with acute myocarditis and infiltrating cells expressing Va7 and Va3 were found in two of eight and one of eight hearts, respectively. Restricted TCR Va as well as V p repertoires indicate that a specific antigen, in the heart was targeted, presented at the groove of major histocompatibility complex molecules. These findings raise the possibility of specific immunotherapy with synthetic TCR V a or V p peptides to prevent T-cell-mediated myocardial damage in patients with viral myocarditis.
📜 SIMILAR VOLUMES
T-cell-mediated myocardial damage has been shown to be involved in acute myocarditis and dilated cardiomyopathy. It is necessary for T-cells to receive a co-stimulatory signal as well as the main signal through the T-cell receptor for antigen-specific T-cell activation to occur. To investigate the r