The Journal of Experimental Medicine
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Published 4 March 2002. doi:10.1084/jem.20011786
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© Rockefeller University Press, 0022-1007/2002/3/625/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 5, March 4, 2002 625-636

Original Article

Functionally Distinct Subsets of CD1d-restricted Natural Killer T Cells Revealed by CD1d Tetramer Staining

Jenny E. Gumperz1, Sachiko Miyake2, Takashi Yamamura2 and Michael B. Brenner1

1 Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, One Jimmy Fund Way, Boston, MA 02115
2 Department of Immunology, National Institute of Neuroscience, NCNP, Tokyo 187-8502, Japan

Address correspondence to Michael Brenner, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Smith Bldg., 5th Floor, One Jimmy Fund Way, Boston, MA 02115. Phone: 617-525-1000; Fax: 617-525-1010; E-mail: mbrenner{at}rics.bwh.harvard.edu

CD1d-restricted natural killer (NK)T cells are known to potently secrete T helper (Th)1 and Th2 cytokines and to mediate cytolysis, but it is unclear how these contrasting functional activities are regulated. Using lipid antigen–loaded CD1d tetramers, we have distinguished two subsets of CD1d-restricted T cells in fresh peripheral blood that differ in cytokine production and cytotoxic activation. One subset, which was CD4-, selectively produced the Th1 cytokines interferon {gamma} and tumor necrosis factor {alpha}, and expressed NKG2d, a marker associated with cytolysis of microbially infected and neoplastic cells. This subset up-regulated perforin after exposure to interleukin (IL)-2 or IL-12. In contrast, CD4+ CD1d-restricted NKT cells potently produced both Th1 and Th2 cytokines, up-regulated perforin in response to stimulation by phorbol myristate acetate and ionomycin but not IL-2 or IL-12, and could be induced to express CD95L. Further, for both CD1d-restricted NKT cell subsets, we found that antigenic stimulation induced cytokine production but not perforin expression, whereas exposure to inflammatory factors enhanced perforin expression but did not stimulate cytokine production. These results show that the various activities of CD1d-restricted T cells in tumor rejection, autoimmune disease, and microbial infections could result from activation of functionally distinct subsets, and that inflammatory and antigenic stimuli may influence different effector functions.

Key Words: Th1/Th2 cytokines • cytotoxic T cells • lipid antigens • autoimmune disease • cancer


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