Abstract
One of the major mechanisms of tumor escape is the inability of antigen presenting cells (APC), and specifically the most potent APC dendritic cells (DC), to induce potent antitumor immune response. The defects in APC are caused by the variety of tumor-derived factors. In this review we will discuss recent findings which indicate that the members of the family of signal transducers and activators of transcription (STATs), and more specifically STAT3, could be responsible for the abnormal DC differentiation and function in cancer. The different approaches to pharmacological regulation of this pathway and their effects on DC function and antitumor immune responses will be discussed.
Keywords: Dendritic cells, T cells, Jak, STAT
Current Cancer Drug Targets
Title: Targeting of Jak/STAT Pathway in Antigen Presenting Cells in Cancer
Volume: 7 Issue: 1
Author(s): Yulia Nefedova and Dmitry I. Gabrilovich
Affiliation:
Keywords: Dendritic cells, T cells, Jak, STAT
Abstract: One of the major mechanisms of tumor escape is the inability of antigen presenting cells (APC), and specifically the most potent APC dendritic cells (DC), to induce potent antitumor immune response. The defects in APC are caused by the variety of tumor-derived factors. In this review we will discuss recent findings which indicate that the members of the family of signal transducers and activators of transcription (STATs), and more specifically STAT3, could be responsible for the abnormal DC differentiation and function in cancer. The different approaches to pharmacological regulation of this pathway and their effects on DC function and antitumor immune responses will be discussed.
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Cite this article as:
Nefedova Yulia and Gabrilovich I. Dmitry, Targeting of Jak/STAT Pathway in Antigen Presenting Cells in Cancer, Current Cancer Drug Targets 2007; 7 (1) . https://dx.doi.org/10.2174/156800907780006887
DOI https://dx.doi.org/10.2174/156800907780006887 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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