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-Galactosylceramide Specifically Stimulates V14+ NK T Lymphocytes1
*
Division of Developmental Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121;
Pharmaceutical Research laboratory, Kirin Brewery Co., Takasaki-shi, Gumna, Japan;
Department of Immunology and Infectious Diseases, Harvard School of Public Health, and Department of Medicine, Harvard Medical School, Boston, MA 02115;
§
Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, PA 19111; and
¶
CREST (Core Research for Evolutional Science and Technology) Project, Japan Science and Technology Corporation and Division of Molecular Immunology, Center for Biomedical Science, School of Medicine, Chiba University, Chuo, Chiba, Japan
Mouse CD1 (mCD1) glycoproteins are known to present peptides, while
human CD1 molecules present glycolipids. In mice, mCD1-autoreactive NK
T cells play critical roles in various immune responses, through the
secretion of high amounts of cytokines. This study was initiated to
determine whether glycolipids are involved in the autorecognition of
mCD1 by NK T cells. 
-Galactosylceramide (-GalCer) was the only
glycolipid tested capable of eliciting an mCD1-restricted response by
splenic T cells. Moreover, splenic T cells derived from mCD1-deficient
mice were not stimulated by -GalCer, suggesting that the responsive
T cells are selected by mCD1. Using cytoflow techniques, we confirmed
that, in response to -GalCer, IFN-
-secreting cells displayed an
NK T cell phenotype. The predominance of IFN- vs IL-4, however, is
determined by the type of mCD1+ APC, suggesting the
potential for APC regulation of cytokine production by NK T cells.
Among a panel of 10 mCD1-autoreactive T cell hybridomas, only the ones
that express the typical V14J281 TCR rearrangement of NK T cells
responded to -GalCer. Fixation or treatment of mCD1+
APCs with an inhibitor of endosomal acidification and the use of mCD1
mutants unable to traffic through endosome still allowed -GalCer to
stimulate NK T cells. Thus, endosomal trafficking and Ag processing are
not required for glycolipid recognition. In summary, -GalCer might
be the autologous ligand, or a mimic of a glycolipid ligand, involved
in the mCD1-mediated stimulation of NK T cells.
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