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
Expression of cytokine mRNAs in murine hearts with acute myocarditis caused by coxsackievirus B3
β Scribed by Seko, Yoshinori; Takahashi, Naoyuki; Yagita, Hideo; Okumura, Ko; Yazaki, Yoshio
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 109 KB
- Volume
- 183
- Category
- Article
- ISSN
- 0022-3417
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β¦ Synopsis
In murine acute viral myocarditis, natural killer (NK) cells infiltrate the heart first, followed by activated T-cells, which play an important role in the pathogenesis of the myocardial damage. Because of their multipotential effects, cytokines are thought to play a role in the induction and development of these immune processes. To clarify in more detail the precise mechanism of the cytokine networks involved, the expression of various cytokine mRNAs has been investigated in myocardial cells infected with Coxsackievirus B3 (CVB3) in vivo and in vitro by a semiquantitative polymerase chain reaction (PCR) method. Interleukin (IL)-1 alpha, IL-1 beta, IL-6, tumour necrosis factor (TNF)-alpha, and TNF-beta were expressed almost throughout the early phase of virus infection with some variations. IL-2, IL-3, IL-4, IL-10, interferon (IFN)-gamma, granulocyte/macrophage colony stimulating factor (GM-CSF), and IL-2 receptor (IL-2R) were mainly expressed by the infiltrating cells. TNF-alpha, TNF-beta, and IL-1 beta were also expressed partly by the infiltrating cells. T-helper (Th)1-related cytokines (IL-2, IFN-gamma, and TNF-beta) were more strongly expressed than Th2-related cytokines (IL-4 and IL-10) in vivo, indicating that the Th cells which infiltrated the heart and mediated the immune responses in the early phase of acute myocarditis were mainly of Th1-type.
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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 infilt
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
## Abstract Increased expression of inducible nitric oxide synthase (iNOS) has been found in inflammatory myocardial disease and increased production of nitric oxide (NO) has both an inhibitory effect on virus replication and a cytotoxic effect on host cells. To investigate the relationship between