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Department of Molecular Biology, Molecular Immunology Unit, Flanders Interuniversity Institute for Biotechnology and University of Ghent, Ghent, Belgium
IL-15 shows functional redundancy with IL-2 due to its usage of the
ß and 
c subunit of the IL-2R. Yet, the
requirement of IL-15 for an IL-15R
chain for high affinity
interaction and the separate cellular sources of IL-2 and IL-15 suggest
divergent activities for both cytokines. We compared the
growth-inducing and proapoptotic or antiapoptotic activities of IL-15
and IL-2 on mature CD4+ T lymphocytes in the presence or
absence of TCR occupancy. We found that the nature of IL-15 activity
was critically dependent on the activation status of the T cells. In
the absence of TCR triggering, IL-15 did not exert the growth factor
activity of IL-2, but induced a quiescent phenotype, characterized by
maintenance of the cells in the G0/G1 phase of
the cell cycle and down-regulation of CD25, CD71, and CD95 expression.
In the presence of appropriate TCR engagement, the IL-15-induced
quiescent T cells were resistant against TCR-induced cell death and
proliferated strongly. IL-2-treated cells, on the contrary, were
sensitized to cell death, resulting in a negative feedback on cellular
expansion and weak proliferative responsiveness. Consecutive action of
IL-15 during the distinct phases of an in vitro immune response
markedly increased the cell output of a second antigenic stimulation,
as compared with IL-2. These results imply that during immune
reactivity in vivo, IL-15 may take over from the transiently available
IL-2 the role of survival factor but not of growth factor, hence
promoting the long term maintenance of resting, Ag-experienced
CD4+ T cells.
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