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Int J Mol Sci. 2018 Jun 19;19(6). pii: E1803. doi: 10.3390/ijms19061803.

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

Author information

1
Department of Immuno-Oncology, Beckman Research Institute at City of Hope Comprehensive Cancer Center, Duarte, 91010 CA, USA. yulsu@coh.org.
2
Department of Immuno-Oncology, Beckman Research Institute at City of Hope Comprehensive Cancer Center, Duarte, 91010 CA, USA. shbanerjee@coh.org.
3
Department of Immuno-Oncology, Beckman Research Institute at City of Hope Comprehensive Cancer Center, Duarte, 91010 CA, USA. sewhite@coh.org.
4
Department of Immuno-Oncology, Beckman Research Institute at City of Hope Comprehensive Cancer Center, Duarte, 91010 CA, USA. mkortylewski@coh.org.

Abstract

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.

KEYWORDS:

STAT3; immunosuppression; myeloid cells

PMID:
29921770
PMCID:
PMC6032252
DOI:
10.3390/ijms19061803
[Indexed for MEDLINE]
Free PMC Article

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