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-Dependent and IFN--Independent Induction of Apoptosis1
Department of Clinical and Biological Sciences, University of Turin, Orbassano, Italy
Human normal and malignant T cells cease to proliferate,
down-modulate Bcl-2 expression, and undergo apoptosis when cultured in
the presence of NO-donor compounds (sodium nitroprusside and NOC12) for
48 h. At 72 h, cells that evade apoptosis start to
proliferate again, overexpress both chains of the IFN-
R, and thus
become susceptible to apoptosis in the presence of IFN-. By
contrast, in the presence of IFN-, no apoptosis, but an increase of
proliferation was displayed by control cultures of T cells not exposed
to NO and not overexpressing IFN-R chains. The NO-induced cell
surface overexpression of IFN-R chains did not affect the
transduction of IFN--mediated signals, as shown by the expression of
the transcription factor IFN regulatory factor 1 (IRF-1). However,
transduction of these signals was quantitatively modified, because
IFN- induces enhanced levels of caspase-1 effector death in
NO-treated cells. These findings identify NO as one of the
environmental factors that critically govern the response of T cells to
IFN-. By inducing the overexpression of IFN-R chains, NO decides
whether IFN- promotes cell proliferation or the induction of
apoptosis.
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