The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/7/109/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 1, July 7, 1997 109-120

Articles

Requirements for CD1d Recognition by Human Invariant V{alpha}24+ CD4–CD8– T Cells

Mark Exley*, Jorge Garcia*, Steven P. Balk*, and Steven Porcelli{ddagger}

From the * Cancer Biology Program, Hematology/Oncology Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215; and {ddagger} Lymphocyte Biology Section, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115

A subset of human CD4–CD8– T cells that expresses an invariant V{alpha}24-J{alpha}Q T cell receptor (TCR)-{alpha} chain, paired predominantly with Vβ11, has been identified. A series of these V{alpha}24 Vβ11 clones were shown to have TCR-β CDR3 diversity and express the natural killer (NK) locus–encoded C-type lectins NKR-P1A, CD94, and CD69. However, in contrast to NK cells, they did not express killer inhibitory receptors, CD16, CD56, or CD57. All invariant V{alpha}24+ clones recognized the MHC class I–like CD16 molecule and discriminated between CD1d and other closely related human CD1 proteins, indicating that recognition was TCR-mediated. Recognition was not dependent upon an endosomal targeting motif in the cytoplasmic tail of CD1d. Upon activation by anti-CD3 or CD1d, the clones produced both Th1 and Th2 cytokines. These results demonstrate that human invariant V{alpha}24+ CD4–CD8– T cells, and presumably the homologous murine NK1+ T cell population, are CD1d reactive and functionally distinct from NK cells. The conservation of this cell population and of the CD1d ligand across species indicates an important immunological function.

Address correspondence to Steven Porcelli, Lymphocyte Biology Section, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, 250 Longwood Ave., Boston, MA 02115; Phone: 617-432-4984; FAX: 617-667-0610; or Steven P. Balk, Hematology/Oncology Division, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215. Phone: 617-667-0600; FAX: 617-667-0610.

For antibodies and cell reagents we wish to thank Drs. L. Lanier, A. Lanzavecchia, M. Robertson, J. Ritz, H. Spits, E. Reinherz, D. Olive, and R.G. Kurrle. We also thank other members of the Lymphocyte Biology Section and Geoffrey Sunshine for advice, and Alexis Fertig for technical assistance.

1Abbreviations used in this paper: CHO, Chinese hamster ovary; DN, double negative; KIR, killer cell inhibitory receptor; RT, reverse transcriptase.


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