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J. Exp. Med.,
Volume 189, Number 3, February 1, 1999 521-530
By
§¶
¶
From the * Howard Hughes Medical Institute, Department of Medicine, National Jewish Medical and
Research Center, Denver, Colorado 80206; and the Antigen injection into animals causes antigen-specific T cells to become activated and, rapidly
thereafter, die. This antigen-induced death is inhibited by inflammation. To find out how inflammation has this effect, various cytokines were tested for their ability to interfere with the
rapid death of activated T cells. T cells were activated in vivo, isolated, and cultured with the
test reagents. Two groups of cytokines were active, members of the interleukin 2 family and
the interferons (IFNs) Department of Biochemistry Biophysics and
Genetics, the § Department of Immunology, the Department of Pharmacology, and the ¶ Department of
Medicine, University of Colorado Health Sciences Center, Denver, Colorado 80262
and 
. This activity of IFN-/ has not been described previously. It
was due to direct effects of the IFNs on the T cells and was not mediated by induction of a second cytokine such as interleukin 15. IFN-
did not slow the death of activated T cells, and
therefore the activity of IFN-/ was not mediated only by activation of Stat 1, a protein that
is affected by both classes of IFN. IFN-/ did not raise the levels of Bcl-2 or Bcl-XL in T cells.
Therefore, their activity was distinct from that of members of the interleukin 2 family or CD28
engagement. Since IFN-/ are very efficiently generated in response to viral and bacterial infections, these molecules may be among the signals that the immune system uses to prevent activated T cell death during infections.
;
apoptosis;
interferon type I;
cell survival;
T cell
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