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Center for Immunology and Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455
CD8+ T cells stimulated in vitro with anti-TCR mAb
and B7-1 or ICAM-1 produce IL-2 and clonally expand. Effector function
is acquired within 3 days, but proliferation ceases and the cells begin
to die by apoptosis. Stimulation in vivo with B7-1-expressing
allogeneic tumor results in the same sequence of events with a
comparable time course. In both cases, the cells become anergic within
3 or 4 days of responding; they can no longer respond by producing IL-2
and proliferating, but can still be stimulated to proliferate in
response to exogenous IL-2. This activation-induced nonresponsiveness
(AINR) is not simply a consequence of ongoing cell death; cytokines
that promote survival (IL-7 or IFN-
) or proliferation (human IL-2)
do not restore the ability to produce IL-2 in response to
costimulation. Although similar to the anergy described for
CD4+ T cell clones, AINR differs in that it results from an
initial stimulation with both signal 1 and signal 2. AINR appears to be
an aspect of the normal differentiation of fully stimulated
CD8+ T cells. It is probably important in regulating CTL
responses; it limits the initial T helper-independent response and
converts it to a response that requires T cell help to be sustained and
further expanded. When the initial helper-independent response is not
sufficient to clear Ag, and if help is not available, AINR likely
results in tolerance to the Ag.
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