STAT3 in Tumor-Associated Myeloid Cells: Multitasking to Disrupt Immunity

Myeloid immune cells, such as dendritic cells, monocytes, and macrophages, play a central role in the generation of immune responses and thus are often either disabled or even hijacked by tumors. These new tolerogenic activities of tumor-associated myeloid cells are controlled by an oncogenic transc...

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Bibliographic Details
Published in:International journal of molecular sciences 2018-06, Vol.19 (6), p.1803
Main Authors: Su, Yu-Lin, Banerjee, Shuvomoy, White, Seok Voon, Kortylewski, Marcin
Format: Article
Language:English
Subjects:
Antigen presentation
Antigens
Cancer
Cancer therapies
Cytokines
Cytotoxicity
Dendritic cells
Immune system
Immunity
Immunostimulation
Immunotherapy
Kinases
Leukemia
Lymphocytes
Macrophages
Monocytes
Multitasking
Myeloid cells
Neutrophils
Review
Stat3 protein
Transcription factors
Tumors
Vascular endothelial growth factor
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Summary:Myeloid immune cells, such as dendritic cells, monocytes, and macrophages, play a central role in the generation of immune responses and thus are often either disabled or even hijacked by tumors. These new tolerogenic activities of tumor-associated myeloid cells are controlled by an oncogenic transcription factor, signal transducer and activator of transcription 3 (STAT3). STAT3 multitasks to ensure tumors escape immune detection by impairing antigen presentation and reducing production of immunostimulatory molecules while augmenting the release of tolerogenic mediators, thereby reducing innate and adaptive antitumor immunity. Tumor-associated myeloid cells and STAT3 signaling in this compartment are now commonly recognized as an attractive cellular target for improving efficacy of standard therapies and immunotherapies. Hereby, we review the importance and functional complexity of STAT3 signaling in this immune cell compartment as well as potential strategies for cancer therapy.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms19061803