Expression of CD95 ligand on parenchymal, epithelial, or tumor cells has be
en suggested to downregulate the immune response and to control lymphocyte
activation. Suppression might be mediated by induction of apoptosis or by i
nhibition of Ca2+ channels upon CD95 triggering. We, therefore, aimed to em
ploy this model to modify the immune response to an antigen presented to cy
totoxic T cells by antigen-presenting MC57 cells. This model would be very
useful to specifically downregulate the immune response to autoantigens in
autoimmune situations. However, cytotoxic T cell lines tested in the presen
t study were resistant to CD95 ligand expression on antigen-presenting MC57
cells. In addition, coincubation of the lymphocytes with antigen presentin
g cells failed to block cytotoxicity mediated by the T lymphocytes. We, the
refore, conclude that single expression of CD95 ligand on antigen-presentin
g cells is insufficient to specifically downregulate an immune response by
CD8+- triggered immune response. (C) 2000 Academic Press.