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

Author

Listed:
  • 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)

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.

Suggested Citation

  • 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 & Laurent Galibert, 1997. "A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function," Nature, Nature, vol. 390(6656), pages 175-179, November.
  • Handle: RePEc:nat:nature:v:390:y:1997:i:6656:d:10.1038_36593
    DOI: 10.1038/36593
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    Cited by:

    1. Nils-Petter Rudqvist & Maud Charpentier & Claire Lhuillier & Erik Wennerberg & Sheila Spada & Caroline Sheridan & Xi Kathy Zhou & Tuo Zhang & Silvia C. Formenti & Jennifer S. Sims & Alicia Alonso & Sa, 2023. "Immunotherapy targeting different immune compartments in combination with radiation therapy induces regression of resistant tumors," Nature Communications, Nature, vol. 14(1), pages 1-23, December.
    2. Yuanyuan Luan & Yan Fang & Lin Jiang & Yuehui Ma & Shangjie Wu & Junwen Zhou & Yabin Pu & Qianjun Zhao & Xiaohong He, 2022. "Landscape of Global Gene Expression Reveals Distinctive Tissue Characteristics in Bactrian Camels ( Camelus bactrianus )," Agriculture, MDPI, vol. 12(7), pages 1-15, July.
    3. Wen-Hung Huang & Mei-Ching Yu & Jeng-Yi Huang & Ping-Chin Lai, 2013. "Impact of Hepatitis C Virus Infection on Bone Mineral Density in Renal Transplant Recipients," PLOS ONE, Public Library of Science, vol. 8(5), pages 1-8, May.
    4. Mengyu Liao & Xu Zhu & Yumei Lu & Xiaoping Yi & Youhui Hu & Yumeng Zhao & Zhisheng Ye & Xu Guo & Minghui Liang & Xin Jin & Hong Zhang & Xiaohong Wang & Ziming Zhao & Yupeng Chen & Hua Yan, 2024. "Multi-omics profiling of retinal pigment epithelium reveals enhancer-driven activation of RANK-NFATc1 signaling in traumatic proliferative vitreoretinopathy," Nature Communications, Nature, vol. 15(1), pages 1-16, December.
    5. Sushila Maharjan & Bijay Singh & Jin-Duck Bok & Jeong-In Kim & Tao Jiang & Chong-Su Cho & Sang-Kee Kang & Yun-Jaie Choi, 2014. "Exploring Codon Optimization and Response Surface Methodology to Express Biologically Active Transmembrane RANKL in E. coli," PLOS ONE, Public Library of Science, vol. 9(5), pages 1-15, May.

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