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*
Centre National de la Recherche Scientifique, UMR 8603, Université René Descartes, Paris V, and
Institut National de la Santé et de la Recherche, Unité 25, Hôpital Necker, Paris, France; and
Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd., Gunma, Japan
NK T lymphocytes are characterized by their ability to promptly
generate IL-4 and IFN-
upon TCR engagement. Here, we demonstrate
that these cells can also be fully activated in the absence of TCR
cross-linking in response to the proinflammatory cytokine IL-18
associated with IL-12. NK T cells stimulated with IL-18 plus IL-12
proliferated, killed Fas+ target cells, and produced high
levels of IFN- without IL-4. In these conditions, IFN- production
was at least 10-fold higher than that upon TCR cross-linking.
Interestingly, a 2-h pretreatment with IL-12 plus IL-18 sufficed to
maintain the high IFN--producing potential during subsequent
stimulation with anti-TCR mAbs or with the specific Ag
-galactosylceramide. Similar effects were observed in vivo, because
splenic CD4+ NK T cells from MHC class II-deficient mice
secreted IFN- without further stimulation when removed 2 h
after a single injection of IL-12 plus IL-18. In conclusion, our
evidence for activation of NK T lymphocytes in response to IL-18 plus
IL-12 in the absence of TCR engagement together with the maintenance of
preferential IFN- vs IL-4 production upon subsequent exposure to
specific Ags is consistent with the active participation of this cell
population in innate as well as acquired cellular immune
responses.
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