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Blood, Vol. 92 No. 11 (December 1), 1998:
pp. 4212-4219
Interleukin-6 (IL-6) Prevents Activation-Induced Cell Death:
IL-2-Independent Inhibition of Fas/fasL Expression and Cell Death
Emira Ayroldi,
Ornella Zollo,
Lorenza Cannarile,
Francesca D'
Adamio,
Ursula Grohmann,
Domenico V. Delfino, and
Carlo Riccardi
From the Pharmacology Section, the Department of Clinical and
Experimental Medicine and the Department of Experimental Medicine,
University of Perugia, Perugia, Italy.
Triggering of the TCR/CD3 complex with specific antigen or anti-CD3
monoclonal antibody initiates activation-induced cell death (AICD) in
mature T cells, an effect also mediated by the Fas/FasL system. We have
previously shown that CD2 stimulation rescues T cells from
TCR/CD3-induced apoptosis by decreasing the expression of Fas and FasL.
In the present study, we examined whether the endogenous production of
IL-2 plays a role in the effects mediated by CD2 triggering. The
results indicated that transcription of Fas/FasL is controlled by
interleukin-2 (IL-2) production and that CD2 triggering rescues a
T-cell hybridoma from AICD via decreased production of IL-2. To
ascertain whether modulation of IL-2 may be a general mechanism of AICD
control, we examined other stimuli, capable of modulating the
expression of the Fas/FasL system and the ensuing AICD, for ability to
affect production of IL-2. We found that IL-6 reduced the level of
TCR/CD3-induced apoptosis and the expression of Fas/FasL, yet failed to
inhibit IL-2 production. Because IL-2 is involved in both apoptosis and activation events, these results indicate that, in contrast to CD2,
which inhibits apoptosis and T cell activation, IL-6 inhibits apoptosis
but not IL-2-induced activation. These observations may provide the
basis for differential control of T-cell activation and apoptosis.
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