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1
Trudeau Institute, Saranac Lake, NY 12983
We have previously shown that systemic staphylococcal enterotoxin A
(SEA) injections cause CD4 T cells in TCR-transgenic mice to become
tolerant to subsequent ex vivo restimulation. An active
IFN-
-dependent mechanism of suppression was responsible for the
apparent unresponsiveness of the CD4 T cells. In this study, we analyze
the response of CD4 T cells isolated throughout the first 10 days of
the in vivo response to injected SEA. We show that CD4 T cells isolated
at the peak of the in vivo response undergo very little
activation-induced cell death after sterile FACS sorting or
restimulation in the presence of neutralizing Abs to IFN-. We also
show that the IFN--dependent tolerance develops soon after SEA
injection in the spleens of both normal and TCR-transgenic mice. This
suppression is dependent upon myeloid cells from the SEA-treated mice
and is optimal when inducible NO synthase activity and reactive oxygen
intermediates are both present. The data indicate that IFN-, myeloid
cells, and a combination of NO and reactive oxygen intermediates all
contribute to a common pathway of T cell death that targets activated
or responding CD4 T cells. Sorted Gr-1+ cells from
SEA-treated mice also directly suppress the response of naive CD4 T
cells in mixed cultures, indicating that this tolerance mechanism may
play a role in down-regulating other vigorous immune
responses.
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