A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function

Dirk M. Anderson (), Eugene Maraskovsky, William L. Billingsley, William C. Dougall, Mark E. Tometsko, Eileen R. Roux, Mark C. Teepe, Robert F. DuBose, David Cosman and Laurent Galibert
Additional contact information
Dirk M. Anderson: Departments of Molecular Biology
Eugene Maraskovsky: Immunobiology
William L. Billingsley: Departments of Molecular Biology
William C. Dougall: Departments of Molecular Biology
Mark E. Tometsko: Departments of Molecular Biology
Eileen R. Roux: Immunobiology
Mark C. Teepe: Immunobiology
Robert F. DuBose: Bioinformatics, Immunex Corporation
David Cosman: Departments of Molecular Biology
Laurent Galibert: Departments of Molecular Biology

Nature, 1997, vol. 390, issue 6656, 175-179

Abstract: Abstract Dendritic cells are rare haematopoietic cells that reside in a number of organs and tissues. By capturing, processing and presenting antigens to T cells, dendritic cells are essential for immune surveillance and the regulation of specific immunity1,2,3,4. Several members of the tumour necrosis factor receptor (TNFR) superfamily are integral to the regulation of the immune response. These structurally related proteins modulate cellular functions ranging from proliferation and differentiation to inflammation and cell survival or death5,6. The functional activity of dendritic cells is greatly increased by signalling through the TNFR family member CD40 (refs 7, 8). Here we report the characterization of RANK (for receptor activator of NF-κB), a new member of the TNFR family derived from dendritic cells, and the isolation of a RANK ligand (RANKL) by direct expression screening. RANKL augments the ability of dendritic cells to stimulate naive T-cell proliferation in a mixed lymphocyte reaction, and increases the survival of RANK+T cells generated with interleukin-4 and transforming growth factor (TGF)-β. Thus RANK and RANKL seem to be important regulators of interactions between T cells and dendritic cells.

Date: 1997
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DOI: 10.1038/36593

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