Volume 7 Supplement 2

São Paulo Advanced School of Comparative Oncology: Abstracts

Open Access

Inflammation, immune suppression, and tumor progression

BMC Proceedings20137(Suppl 2):K20

DOI: 10.1186/1753-6561-7-S2-K20

Published: 4 April 2013

The tumor microenvironment is a complex milieu of tumor and host cells. Host cells can include tumor-reactive T cells capable of killing tumor cells. However, more frequently tumor and host components interact to generate a highly immune suppressive environment that frustrates T cell cytotoxicity and promotes tumor progression through a variety of immune and non-immune mechanisms. Myeloid-derived suppressor cells (MDSC) are a major host component contributing to the immune suppressive environment. MDSC accumulate in most patients and experimental mice with cancer. They inhibit both adaptive and innate immunity through a diverse array of suppressive mechanisms and therefore are a significant obstacle for natural immunity and for active cancer immunotherapies. Their accumulation and suppressive potency are driven by pro-inflammatory mediators. In addition to their inherent immune suppressive function, MDSC amplify the immune suppressive activity of macrophages and dendritic cells via cross-talk which results in the up-regulation of inflammatory mediators. Cross-talk between MDSC and other myeloid cells is itself enhanced by inflammation, resulting in an autocrine tumor microenvironment that sustains and amplifies immune suppression. This talk will describe the cell-cell interactions used by MDSC to inhibit anti-tumor immunity and promote tumor progression, and the role of inflammation in promoting cross-talk between MDSC and other cells in the tumor microenvironment.

Declarations

Acknowledgements

Supported by NIH R01CA84232; RO1CA115880.

Authors’ Affiliations

(1)
Dept. Biological Sciences, University of Maryland Baltimore County

Copyright

© Ostrand-Rosenberg; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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