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CUTTING EDGE |





Department of Immunology, Niigata University School of Medicine, Niigata, Japan;
*
Department of Immunology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan;
Core Research for Evolutional Science and Technology (CREST) of Japan Science and Technology (JST) Corporation, Tokyo, Japan; and
Howard Hughes Medical Institute, Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232
CD1-dependent NK1+ T cells rapidly produce
IL-4 upon stimulation through the TCR. These cells may therefore play
an important role in the initiation of Th2 responses. Here, we show
that NK1+ T cells constitutively express receptors for
IL-12 and IFN-
, and that IL-12 induces production of perforin in
these cells. Moreover, while IL-12 induces high levels of IFN-
and
cytotoxic activity of hepatic or splenic mononuclear cells against
tumor cells, this effect of IL-12 is significantly reduced in
CD1-deficient mice with impaired NK1+ T cells development.
These results indicate that NK1+ T cells play a critical
role in IL-12-induced production of IFN-
to initiate Th1 immune
responses and as IL-12-induced cytotoxic effector cells to initiate
antitumor immunity.
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