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B and AP-1 trans-Activation in Response to Minimal TCR Engagement by a Partial Agonist in Naive CD8 T Cells1
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Centre d’Immunologie, Institut National de la Santé et de la Recherche Médicale- Centre National de la Recherche Scientifique (INSERM-CNRS) de Marseille-Luminy, Marseille, France; and
Section of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06517
We investigated the basis for partial reactivity of naive CD8 T
cells expressing an alloreactive transgenic TCR in response to a mutant
alloantigen. When unstimulated APCs were used, IFN-
as well as IL-2
and cell proliferation were observed in response to wild-type Ag,
whereas mutant Ag induced only IFN-. DNA binding and reporter gene
assays showed that the response to mutant Ag involved NF-
B, but not
AP-1 activation, whereas wild-type Ag activated both transcription
factors. Increasing the contribution of costimulatory signals by using
LPS-activated APCs partially corrected the activation by mutant Ag,
because proliferation and weak IL-2 production could be measured. This
also led to AP-1 activation, albeit with delayed kinetics, in response
to mutant Ag. To explain how engagement of the same TCR by distinct
ligands results in different T cell responses, it may be proposed, in
line with models stressing the importance of the kinetics of Ag/TCR
interaction, that two types of signals be distinguished: a "fast"
short-lived signal is sufficient to activate NF-B; whereas a
"slow" signal obtained after prolonged TCR engagement is required
for AP-1 activation. Failure to activate AP-1 in limiting conditions
(unstimulated mutant APC) was partially corrected by increasing
costimulation.
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