Human Dendritic Cells Mediate Cellular Apoptosis via Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand (Trail)
Autor: | Thomas S. Griffith, Neil A. Fanger, Ken Schooley, Charles R. Maliszewski |
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Rok vydání: | 1999 |
Předmět: |
Cytotoxicity
Immunologic tumor Programmed cell death Immunology Antigen presentation Integrin alphaXbeta2 CD11c TRAIL Biology TNF-Related Apoptosis-Inducing Ligand Antigen Antigens CD Interferon medicine Humans Immunology and Allergy human Antigen Presentation Membrane Glycoproteins Histocytochemistry Tumor Necrosis Factor-alpha apoptosis hemic and immune systems Dendritic Cells Flow Cytometry Receptors Interleukin-3 Cell biology Apoptosis Cancer cell Cytokines Original Article Tumor necrosis factor alpha Interferons Apoptosis Regulatory Proteins medicine.drug |
Zdroj: | The Journal of Experimental Medicine |
ISSN: | 1540-9538 0022-1007 |
Popis: | TRAIL (TNF-related apoptosis-inducing ligand) is a member of the TNF family that induces apoptosis in a variety of cancer cells. In this study, we demonstrate that human CD11c(+) blood dendritic cells (DCs) express TRAIL after stimulation with either interferon (IFN)-gamma or -alpha and acquire the ability to kill TRAIL-sensitive tumor cell targets but not TRAIL-resistant tumor cells or normal cell types. The DC-mediated apoptosis was TRAIL specific, as soluble 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 target cells, demonstrating a clear functional difference between the CD11c(+) DC and IL-3Ralpha(+) pre-DC subsets. These results indicate that TRAIL may serve as an innate effector molecule on CD11c(+) DCs for the elimination of spontaneously arising tumor cells and suggest a means by which TRAIL-expressing DCs may regulate or eliminate T cells responding to antigen presented by the DCs. |
Databáze: | OpenAIRE |
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