gms | German Medical Science

77th Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

24.05. - 28.05.2006, Mannheim

Head and neck cancer triggers the internalization of TLR3 in natural killer cells

Meeting Abstract

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  • corresponding author Ralph Pries - University of Luebeck, Luebeck, Germany
  • Sandra Wulff - University of Luebeck, Luebeck, Germany
  • Barbara Wollenberg - University of Luebeck, Luebeck, Germany

German Society of Otorhinolaryngology, Head and Neck Surgery. 77th Annual Meeting of the German Society of Otorhinolaryngology, Head and Neck Surgery. Mannheim, 24.-28.05.2006. Düsseldorf, Köln: German Medical Science; 2006. Doc06hno074

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/hno2006/06hno074.shtml

Published: September 7, 2006

© 2006 Pries et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Natural killer (NK) cells play a dominant role in the network of the innate immunity. Via TLR3 NK cells can be efficiently stimulated by dsRNA. In head and neck squamous cell carcinoma (HNSCC) NK cells seem to be strongly impaired but the true mechanisms of immune escape are not sufficiently known to date. It is obvious that the microenvironment of head and neck cancer results in strongly affected immune functions. NK cells play a major role in the local immune response of HNSCC. In this work we show that TLR3 is predominantly expressed on the cell surface of native NK cells and gets rapidly internalized in response to the HNSCC microenvironment. These findings represent a novel immune escape mechanism of head and neck cancer. The internalization of TLR3 in response to HNSCC could as well be observed in fibroblasts expressing heterologous TLR3 protein. Specific stimulation of NK cell TLR3 with its ligand Poly I:C impairs the internalization of this Toll-like receptor and leads to activated NK cells within the HNSCC microenvironment.