Journal of Innate Immunity
Review
The Bidirectional Crosstalk between Human Dendritic Cells and Natural Killer CellsWehner R. · Dietze K. · Bachmann M. · Schmitz M.Institute of Immunology, Medical Faculty, Technical University of Dresden, Dresden, Germany
Dr. Marc Schmitz Institute of Immunology, Medical Faculty Technical University of Dresden, Fetscherstr. 74 DE–01307 Dresden (Germany) Tel. +49 351 458 6501, E-Mail marc.schmitz@tu-dresden.de |
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Abstract
Dendritic cells (DCs) are professional antigen-presenting cells, which display an extraordinary capacity to induce T-cell responses. Recent findings revealed that DCs also play a crucial role in the activation of natural killer (NK) cells representing important effectors in the innate immune defense against viruses and tumors. Here, we summarize various studies investigating the bidirectional crosstalk between human DCs and NK cells. In this context, it has been reported that DCs efficiently enhance CD69 expression, proliferation, interferon (IFN)-γ secretion and cytotoxic activity of NK cells. Cell membrane-associated molecules as well as soluble factors such as interleukin-12, tumor necrosis factor-α and type I IFNs contributed to DC-mediated NK cell activation. Reciprocally, the ability of human NK cells to enhance the immunostimulatory capacity of DCs was shown. Thus, NK cells promoted the maturation of DCs and markedly augmented their capacity to produce proinflammatory cytokines and to stimulate T-cell responses. The NK cell-mediated effects on DCs were dependent on cell membrane-associated molecules such as NKp30 and soluble factors such as tumor necrosis factor-α and IFN-γ. In conclusion, the reciprocal activating interaction between human DCs and NK cells may play a pivotal role in the immune defense against viruses and tumors.
© 2011 S. Karger AG, Basel
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Article / Publication Details
Received: October 21, 2010
Accepted: December 07, 2010
Published online: March 11, 2011
Issue release date: April 2011
Number of Print Pages: 6
Number of Figures: 1
Number of Tables: 0
ISSN: 1662-811X (Print)
eISSN: 1662-8128 (Online)
For additional information: https://www.karger.com/JIN
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