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Inflammatory Mediators Hold the Key to Dendritic Cell Suppression and Tumor Progression

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Cancer has long been considered a disease that is associated with immune tolerance. Its connection with inflammation initially appears paradoxical. During the last decade, it has become increasingly clear that immune infiltrates form an integral part of tumor and critically contribute to its development and progression. In the tumor milieu, a variety of inflammatory mediators, such as cytokines (IL- 6, IL-10, VEGF, TGFβ, M-CSF and GM-CSF), chemokines (CCL20 and CXCL8), hormones (prostanoids like PGE2), reactive oxygen species and cellular constituents (gangliosides), are continuously produced. These mediators represent a critical interface between immune and neoplastic compartments. Not only do they continuously support tumor survival and expansion, but suppress the function of immune cells, notably, dendritic cells - the powerful antigen presenting cells that are crucial for induction of tumor-specific immune responses. This review summarizes such a dual role of inflammatory factors and discusses the controversies associated with specific mediators including IL-10, GM-CSF and ROS in tumor and immune modulation. Identifying the inflammatory signature of cancer patients hence represents a critical task for individualized immunotherapy in the future.

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Keywords: Inflammation; cancer; dendritic cells; immune tolerance; immunotherapeutics; inflammatory mediators; neoplastic compartments; pathogenic threat; tumor; tumor milieu

Document Type: Research Article

Publication date: 2011-12-01

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  • Current Medicinal Chemistry covers all the latest and outstanding developments in medicinal chemistry and rational drug design. Each issue contains a series of timely in-depth reviews written by leaders in the field covering a range of the current topics in medicinal chemistry. Current Medicinal Chemistry is an essential journal for every medicinal chemist who wishes to be kept informed and up-to-date with the latest and most important developments.
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