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*
Biomedical Research Center, Osaka University Medical School, Yamada-oka, Suita, Osaka, Japan; Departments of
Bacteriology and
Immunology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan; and
§
Fujisaki Institute, Hayashibara Biochemical Laboratories, Okayama, Japan
Like IL-12, IFN-
-inducing factor/IL-18 has been shown to
stimulate T cells for IFN- production and growth promotion.
Considering the NK-stimulatory capacity of IL-12, we investigated the
effect of IL-18 on NK lineage cells. A
CD4-CD8-surface
Ig-Ia- fraction of freshly prepared C57BL/6
spleen cells proliferated strikingly in response to combinations of
IL-12 + IL-18 or IL-2 + IL-18, but not to the individual
cytokines or IL-2 + IL-12. Cells proliferating in response to
IL-2 + IL-18 were NK1.1+CD3-, whereas
IL-12 + IL-18-responsive cells were
NK1.1-CD3-. Restimulation of the former cells
with IL-12 + IL-18 or the latter cells with IL-2 + IL-18
resulted in the generation of NK1.1-CD3- or
NK1.1+CD3- cells, respectively. Moreover, a
NK1.1+CD3-CD4-CD8-surface
Ig-Ia- population isolated from spleen cells
was found to form NK1.1+CD3- or
NK1.1-CD3- blasts by stimulation with
IL-2 + IL-18 or IL-12 + IL-18, respectively, and the NK1.1
positivity on these blasts was again reversed after restimulation with
an alternative combined stimulus. Both types of blasts produced
enormously large amounts of IFN- in response to IL-12 + IL-18
and exhibited strikingly high levels of NK activity. These results
indicate that IL-18 plays an obligatory role in inducing proliferation
and activation of
NK1.1+CD3-CD4-CD8-
cells and that the expression of the NK1.1 marker is reversible,
depending on the cytokine used for stimulation in combination with
IL-18.
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