Abstract
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-gamma, and that IL-12 induces production of perforin in these cells. Moreover, while IL-12 induces high levels of IFN-gamma 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-gamma to initiate Th1 immune responses and as IL-12-induced cytotoxic effector cells to initiate antitumor immunity.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Antigens / analysis*
-
Antigens, CD1 / physiology
-
Antigens, Surface
-
Cytotoxicity, Immunologic
-
Fas Ligand Protein
-
Interferon gamma Receptor
-
Interleukin-12 / pharmacology*
-
Lectins, C-Type
-
Liver / cytology
-
Male
-
Membrane Glycoproteins / genetics
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
NK Cell Lectin-Like Receptor Subfamily B
-
Perforin
-
Pore Forming Cytotoxic Proteins
-
Proteins / analysis*
-
Receptors, Interferon / metabolism
-
Receptors, Interleukin / metabolism
-
Receptors, Interleukin-12
-
T-Lymphocyte Subsets / immunology*
-
Up-Regulation
Substances
-
Antigens
-
Antigens, CD1
-
Antigens, Surface
-
Fas Ligand Protein
-
Fasl protein, mouse
-
Lectins, C-Type
-
Membrane Glycoproteins
-
NK Cell Lectin-Like Receptor Subfamily B
-
Pore Forming Cytotoxic Proteins
-
Proteins
-
Receptors, Interferon
-
Receptors, Interleukin
-
Receptors, Interleukin-12
-
Perforin
-
Interleukin-12