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Mary Kirkland Center for Lupus Research, Hospital for Special Surgery, Weill Medical College and Graduate School of Medical Sciences of Cornell University, New York, NY 10021
Self-reactive T cells are present in the mature immune repertoire
as demonstrated by T cell proliferation induced by autologous non-T
cells in the autologous mixed lymphocyte reaction. This reaction
generates regulatory T cells in vitro and may reflect immune regulatory
pathways in vivo, but the antigenic peptides recognized remain
uncharacterized. We revisited this issue in light of the
importance of apoptosis in immune regulation. We found that apoptosis
among peripheral blood non-T stimulator cells is associated with
augmented induction of autologous T cell proliferation. Our data show
that caspase activity in the non-T stimulator population is essential
for induction of autologous T cell proliferation, suggesting that
cellular components in the non-T cell fraction are enzymatically
modified, most likely by effector caspases, and have a direct or
indirect effect on autoreactive T cell activation. Furthermore,
exposure of macrophage-derived dendritic cells to apoptotic non-T cells
augments autologous T cell proliferation, and blockade of
v
5 integrin, but not
v3, inhibits the capacity of irradiated
non-T cells or dendritic cells to stimulate autologous T cell
proliferation. These experiments, using an entirely autologous system,
suggest the interpretation that autoreactive T cells may recognize
self-Ags modified through the actions of caspases and presented to T
cells by dendritic cells. Induction of an in vivo autologous mixed
lymphocyte reaction by caspase-modified self-Ags present in apoptotic
cells may represent a mechanism to maintain peripheral immune
tolerance.
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