Human Dendritic Cells Mediate Cellular Apoptosis via Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL)

doi:10.1084/jem.190.8.1155

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© The Rockefeller University Press, 0022-1007/1999/10/1155/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 8, October 18, 1999 1155-1164

Human Dendritic Cells Mediate Cellular Apoptosis via Tumor Necrosis Factor–related Apoptosis-inducing Ligand (TRAIL)

Neil A. Fanger^a, Charles R. Maliszewski^a, Ken Schooley^b, and Thomas S. Griffith^c
^a Department of Discovery Research, Immunex Corporation, Seattle, Washington 98101
^b Department of Molecular Biology, Immunex Corporation, Seattle, Washington 98101
^c Department of Immunobiology, Immunex Corporation, Seattle, Washington 98101

Correspondence to: Thomas S. Griffith, Dept. of Urology, 428 MRC, University of Iowa, 200 Hawkins Dr., Iowa City, IA 52242-1089. Tel:319-335-7581 Fax:319-356-3900 E-mail:griffitht{at}mail.medicine.uiowa.edu.

TRAIL (TNF-related apoptosis-inducing ligand) is a member ofthe TNF family that induces apoptosis in a variety of cancercells. In this study, we demonstrate that human CD11c⁺ blooddendritic cells (DCs) express TRAIL after stimulation with eitherinterferon (IFN)- ${gamma}$ or - ${alpha}$ and acquire the ability to kill TRAIL-sensitivetumor cell targets but not TRAIL-resistant tumor cells or normalcell types. The DC-mediated apoptosis was TRAIL specific, assoluble TRAIL receptor blocked target cell death. Moreover,IFN-stimulated interleukin (IL)-3 receptor (R) ${alpha}$ ⁺ blood precursor(pre-)DCs displayed minimal cytotoxicity toward the same targetcells, demonstrating a clear functional difference between theCD11c⁺ DC and IL-3R ${alpha}$ ⁺ pre-DC subsets. These results indicatethat TRAIL may serve as an innate effector molecule on CD11c⁺DCs for the elimination of spontaneously arising tumor cellsand suggest a means by which TRAIL-expressing DCs may regulateor eliminate T cells responding to antigen presented by theDCs.

Key Words: TRAIL, apoptosis, tumor, dendritic cells, human

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