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in Response to IL-181
*
Biomedical Research Center, Osaka University Medical School, Osaka, Japan;
Department of Bacteriology and
Department of Immunology, Hyogo College of Medicine, Hyogo, Japan;
§
Genetics Institute Inc., Cambridge, MA 02140; and
¶
Fujisaki Institute, Hayashibara Biochemical Laboratories, Okayama, Japan
IL-12 and IL-18 have the capacity to stimulate IFN-
production
by T cells. Using a T cell clone, we reported that IL-18 responsiveness
is generated only after exposure to IL-12. Here, we investigated the
induction of IL-18 responsiveness in resting CD8+,
CD4+, and CD4-CD8- T cells.
Resting T cells respond to neither IL-12 nor IL-18. After stimulation
with anti-CD3 plus anti-CD28 mAbs, CD8+,
CD4+, and CD4-CD8- T cells
expressed IL-12R, but not IL-18R, and produced IFN- in response to
IL-12. Cultures of T cells with anti-CD3/anti-CD28 in the
presence of rIL-12 induced IL-18R expression and IL-18-stimulated
IFN- production, which reached higher levels than that induced by
IL-12 stimulation. However, there was a substantial difference in the
expression of IL-18R and IL-18-stimulated IFN- production among T
cell subsets. CD4+ cells expressed marginal levels of
IL-18R and produced small amounts of IFN-, whereas CD8+
cells expressed higher levels of IL-18R and produced more IFN- than
CD4+ cells. Moreover, CD4-CD8-
cells expressed levels of IL-18R comparable to those for
CD8+ cells but produced IFN- one order higher than did
CD8+ cells. These results indicate that the induction of
IL-18R and IL-18 responsiveness by IL-12 represents a mechanism
underlying enhanced IFN- production by resting T cells, but the
operation of this mechanism differs depending on the T cell subset
stimulated.
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