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Targeting Functionality of Cancer Cell-Derived Extracellular Vesicles to Immune Cells of the Tumor Microenvironment
Hinrich P Hansen*, Katrin S Reiners and Elke Pogge von StrandmannDepartment of Internal Medicine I, University Clinic Cologne, Cologne, Germany
- *Corresponding Author:
- Hinrich P Hansen
Department of Internal Medicine I
University Clinic Cologne
Cologne, Germany
Tel: +49 221 5808
Email: h.hansen@unikoeln. de
Received Date: April 17, 2015; Accepted Date: May 15, 2015; Published Date: May 18, 2015
Citation: Hansen HP, Reiners KS, Strandmann EPV (2015) Targeting Functionality of Cancer Cell-Derived Evs to Immune Cells of the Tumor Microenvironment. J Clin Exp Pathol 5:226. doi: 10.4172/2161-0681.1000226
Copyright: ©2015 Jeffrey Hansen HP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
In most cases, cancer cells cannot proliferate alone. They receive support form stromal cells and recruit and reprogram non-malignant immune cells not to damage the cancer cells but to support the tumor growth. Classical Hodgkin lymphoma (cHL) is a good example, as its growth critically depends on tumor-supporting immune cells. The affected lymphoid tissue contains very few disseminated malignant Hodgkin- and Reed-Sternberg (H-RS) cells, which are outnumbered by a massive infiltrate of lymphocytes, fibroblasts and innate immune cells. [1]. The H-RS cells need this environment to survive and proliferate because they are usually not detectable in the peripheral blood and they have difficulties to grow in immune-deficient mice [2]. H-RS cells manipulate the bystander cells for better development of their malignant phenotype and evasion of the host defense [3]. Among the infiltrated immune cells, the eosinophils and mast cells play an important role and their cell count indicates a negative prognostic feature [4,5]. In vitro, the direct interaction with cancer cells communicates survival in cancer cells and the production of cancersupporting factors in immune cells. In the last years, extracellular vesicles (EVs) emerged as important vehicles to shuttle between different the cell types and communicate as a surrogate cellular crosstalk in trans [6,7].
