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.
Highlights
In recent years, a number of clinical studies have demonstrated the efficacy of emerging immunotherapies against treatment refractory cancers, thereby gaining the attention of the medical community as well as patients [1,2,3]
Tumor-associated myeloid cells, such as dendritic cells (DCs), macrophages, and myeloid-derived suppressor cells (MDSCs), play a central role in the cellular immune network based on their physiological role in the regulation of tissue homeostasis, immune surveillance, and wound healing
signal transducer and activator of transcription 3 (STAT3) activation, activation, which propagates from cancer cells into non‐malignant immune cells infiltrating tumors, which propagates from cancer cells into non-malignant immune cells infiltrating tumors, is known to is known to play an important role in promoting these tolerogenic effects (Figure 1)
Summary
A number of clinical studies have demonstrated the efficacy of emerging immunotherapies against treatment refractory cancers, thereby gaining the attention of the medical community as well as patients [1,2,3]. As shown in a number of preclinical mouse tumor models and with emerging clinical data, tumor-mediated hijacking of myeloid cell function largely depends on the transcription factor, signal transducer and activator of transcription 3 (STAT3) [7,8]. STAT3 in common and functionally well‐defined STAT3 in genetically stable, tumor‐associated myeloid cells genetically stable, tumor-associated cells providesstrategy for a broadly applicable immunotherapeutic provides for a broadly applicable myeloid immunotherapeutic that could overcome the limitations strategy that could overcome the limitations of current cancer immunotherapies [10,15,16]. In the presence tumor‐derived factors, the normal developmental pathways to mature DCs, M1 macrophages, or of tumor-derived factors, the normal developmental pathways to mature DCs, M1 macrophages, neutrophils are deregulated as indicate by red crosses.
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