The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/9/775/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 6, September 20, 1999 775-782

Original Article

In Vivo Expression of Natural Killer Cell Inhibitory Receptors by Human Melanoma–Specific Cytolytic T Lymphocytes

Daniel E. Speisera, Mikaël J. Pitteta, Danila Valmoria, Rod Dunbarb, Donata Rimoldic, Danielle Liénarda,d, H. Robson MacDonaldc, Jean-Charles Cerottinia,c, Vincenzo Cerundolob, and Pedro Romeroa

a Division of Clinical Onco-Immunology, Ludwig Institute for Cancer Research, Lausanne Branch, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland
b Institute of Molecular Medicine, Nuffield Department of Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DU, United Kingdom
c Ludwig Institute for Cancer Research, Lausanne Branch, 1066 Epalinges, Switzerland
d Multidisciplinary Oncology Center, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland
Division of Clinical Onco-Immunology, Ludwig Institute for Cancer Research, CHUV - BH 19-602, CH-1011 Lausanne, Switzerland.41-21-314-74-7741-21-314-01-82

daniel.speiser{at}hospvd.ch

Natural killer (NK) receptor signaling can lead to reduced cytotoxicity by NK cells and cytolytic T lymphocytes (CTLs) in vitro. Whether T cells are inhibited in vivo remains unknown, since peptide antigen–specific CD8+ T cells have so far not been found to express NK receptors in vivo. Here we demonstrate that melanoma patients may bear tumor-specific CTLs expressing NK receptors. The lysis of melanoma cells by patient-derived CTLs was inhibited by the NK receptor CD94/NKG2A. Thus, tumor-specific CTL activity may be decreased through NK receptor triggering in vivo.

Key Words: cytolytic T lymphocytes • natural killer receptors • melanoma • tumor immunity • peptide antigen

1used in this paper: ILT2, Ig-like transcript 2; NKT cell, NK receptor–positive cell expressing CD3 and/or TCR-{alpha}/β; TILN, tumor-infiltrated LN

© 1999 The Rockefeller University Press


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