Titlebook: Dendritic Cells in Cancer; Russell D. Salter,Michael R. Shurin Book 2009 Springer-Verlag New York 2009 Activation.Cancer.Dendritic Cells.D

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https://doi.org/10.1007/978-3-642-31251-9 of functions generally for the benefit of the host. In cancers, the types, relative proportions, and functions of DC are altered, often to the detriment of the host. This chapter reviews the general issues related to imbalanced DC populations and their causes and dysfunctional consequences in the t

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Interaction of Slow Dissipative Solitudes,ndritic cell differentiation and maturation as well as a direct induction of apoptosis in dendritic cells or their precursors. Numerous experimental and clinical studies revealed that different factors produced by both tumor and stromal cells, such as VEGF, IL-10, TGF-β, gangliosides and other, coul

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Foundations of Reduction Theoryin the remodeling of the peritumoral microenvironment. This recently defined alternative mechanism of intercellular communication is exploited by tumor cells to favor their own growth and survival through the delivery of detrimental signals to the host’s innate and adaptive immune system. Initially

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https://doi.org/10.1007/978-3-642-84230-6 of tumor escape. The defects in dendritic cells are caused primarily by soluble tumor-derived factors. In recent years accumulated evidence suggested that the members of the family of signal transducers and activators of transcription (STAT), and more specifically STAT3, could be primarily responsi

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https://doi.org/10.1007/978-1-84628-517-2es and stress-associated molecules have well-documented effects on the activity of lymphocytes, stress exposure may disrupt processes that occur earlier in the immune response. Stress-induced alterations in immune function may, in part, result from changes in the development and/or function of cells

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