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Ann N Y Acad Sci. 1999;887:181-90.

Apoptosis in coxsackievirus B3-induced myocarditis and dilated cardiomyopathy.

Author information

1
Department of Pathology, University of Vermont, Burlington 05405, USA. shuber(a)salus.uvm.edu

Abstract

Group B coxsackieviruses (CVB), which infect the myocardium, cause myocarditis and dilated cardiomyopathy. However, not all infections of the myocardium result in disease. In the mouse model, CVB infection stimulates autoimmune T cell response to cardiac antigens, and these autoimmune effectors cause myocyte necrosis and cardiomyopathy. Induction of pathogenic autoimmunity depends upon CD4+ Th1 (interferon-gamma positive) cells while Th2 (IL-4 positive) cell responses promote disease resistance. T lymphocytes expressing the gamma-delta T cell receptor (gamma delta +) constitute up to 12% of the inflammatory cells in the heart and are crucial to maintaining a dominant Th1 response phenotype. gamma delta + lymphocytes modulate T cell responses by selectively lysing CD4+ Th2 cells. Th1 cells are not killed by gamma delta + cells. Lysis requires direct cell:cell interaction between the gamma delta + cell and CD4+ Th2 target and is most likely mediated through Fas:FasL interaction. These studies demonstrate a novel mechanism for immune modulation of cytokine responses in vivo.

PMID:
10668474
[Indexed for MEDLINE]

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