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Apoptosis in Coxsackievirus B3‐induced Myocarditis and Dilated Cardiomyopathy
Author(s) -
HUBER S. A.,
BUDD R. C.,
ROSSNER K.,
NEWELL M. K.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07932.x
Subject(s) - coxsackievirus , myocarditis , immunology , dilated cardiomyopathy , autoimmunity , immune system , t cell , interferon , tumor necrosis factor alpha , cytokine , medicine , biology , virus , enterovirus , heart failure
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 + Thl (interferon‐γ positive) cells while Th2 (IL‐4 positive) cell responses promote disease resistance. T lymphocytes expressing the γ‐δ T cell receptor (γδ + ) constitute up to 12% of the inflammatory cells in the heart and are crucial to maintaining a dominant Th1 response phenotype. γδ + lymphocytes modulate T cell responses by selectively lysing CD4 + Th2 cells. Thl cells are not killed by γδ + cells. Lysis requires direct cell:cell interaction between the γδ + 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 .