作者: S A Huber , A Mortensen , G Moulton
DOI: 10.1128/JVI.70.5.3039-3044.1996
关键词: BALB/c 、 Antigen 、 Cytokine 、 Virology 、 CD8 、 Molecular biology 、 Apoptosis 、 Lymphocyte 、 T cell 、 Population 、 Biology 、 Immunology 、 Insect Science 、 Microbiology
摘要: Two variants of coxsackievirus B3 have been used to investigate the pathogenesis myocarditis in BALB/c mice. H3 virus induces moderate and H310A1 minimal myocarditis, although both viruses infect replicate heart. Cells expressing gamma delta+ T-cell receptor composed 5 13% lymphocytes infiltrating hearts virus-infected mice belonged either CD4- CD8+ delta+- or CD8- delta+-cell population. Giving 5,000 cells isolated from recipients restored susceptibility recipient animals shifted pattern cytokine production virus-immune CD4+-cell population being predominantly interleukin-4 producing interferon Apoptosis was evident lymphocyte myocardia by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling assay splenic DNA fragmentation agarose gel electrophoresis confined CD4+ No apoptosis observed mice, but induced subsequent delta +-T-cell transfer. These results are consistent with hypothesis that T may help modulate responses during infections vivo might be involved this modulation.