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Tumor-Derived Factors Responsible for Dendritic Cell Dysfunction

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Abstract

Perpetuation of immune deficiency throughout tumor development is, to a great degree, the result of impairment of dendritic cell function by products secreted by tumors. They include cytokines, non-tumor-specific molecules (gangliosides, prostanoids, nitric oxide, etc.) and tumor-(specific) antigens (MUC-1, PSA, Her-2 neu). They may engender a distortion of dendritic cell development, block dendritic cell maturation, induce dendritic cell apoptosis or interfere with antigen presentation. Identifying those molecules and their interaction with dendritic cells will accelerate the development of more efficient immunotherapies. In this chapter we review the current literature on these interactions and highlight the possible avenues of minimization of their deleterious effects.

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Acknowledgements

APC had been supported by University of Queensland and Paul Mackay Bolton Research Scholarships and is currently recipient of a NHMRC Biomedical Postdoctoral Fellowship ID: 443041. JAL is supported by the National Breast Cancer Foundation and Griffith University.

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  1. Bancroft Centre, L floor, Queensland Institute of Medical Research, Brisbane, QLD 4006, Australia

    Alberto Pinzon-Charry

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  1. Alberto Pinzon-Charry
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  2. J. Alejandro López
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Correspondence to Alberto Pinzon-Charry .

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    Pinzon-Charry, A., López, J.A. (2009). Tumor-Derived Factors Responsible for Dendritic Cell Dysfunction. In: Salter, R., Shurin, M. (eds) Dendritic Cells in Cancer. Springer, New York, NY. https://doi.org/10.1007/978-0-387-88611-4_7

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