Myeloid derived suppressor cells—An overview of combat strategies to increase immunotherapy efficacy

Draghiciu, Oana; Lubbers, Joyce M.; Nijman, Hans W.; Daemen, Toos

doi:10.4161/21624011.2014.954829

Cited by 244 publications

(204 citation statements)

References 79 publications

(107 reference statements)

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“…2). Both IL-1β and PGE2 act as chemoattractants for MDSCs (143). Therefore, tumor cell binding to sICAM-1 results in an amplifying strategy for the recruitment of immune populations to develop an immune tolerant microenvironment in the liver.…”

Section: Tumor Cell Extravasation: Opening the Liver's Doors To Invadmentioning

confidence: 99%

Role of liver ICAM-1 in metastasis

2017

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Abstract. Intercellular adhesion molecule (ICAM)-1, is a transmembrane glycoprotein of the immunoglobulin (Ig)-like superfamily, consisting of five extracellular Ig-like domains, a transmembrane domain and a short cytoplasmic tail. ICAM-1 is expressed in various cell types, including endothelial cells and leukocytes, and is involved in several physiological processes. Furthermore, it has additionally been reported to be expressed in various cancer cells, including melanoma, colorectal cancer and lymphoma. The majority of studies to date have focused on the expression of the ICAM-1 on the surface of tumor cells, without research into ICAM-1 expression at sites of metastasis. Cancer cells frequently metastasize to the liver, due to its unique physiology and specialized liver sinusoid capillary network. Liver sinusoidal endothelial cells constitutively express ICAM-1, which is upregulated under inflammatory conditions. Furthermore, liver ICAM-1 may be important during the development of liver metastasis. Therefore, it is necessary to improve the understanding of the mechanisms mediated by this adhesion molecule in order to develop host-directed anticancer therapies.

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Section: Tumor Cell Extravasation: Opening the Liver's Doors To Invadmentioning

confidence: 99%

Role of liver ICAM-1 in metastasis

2017

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“…20 Another crucial immunosuppressive cell population is represented by MDSCs that inhibit antitumor T-cell responses by multiple mechanisms and can be considered as one of the most important components of tumor-induced immunosuppression in melanoma. 14,15,32,33 It has been previously described that MDSCs accumulate in peripheral lymphoid organs and migrate to tumor sites, where they contribute to immunosuppression. 15,16,33,34 Furthermore, some evidence suggests that MDSCs can induce an expansion of Tregs.…”

Section: Studying Cd4mentioning

confidence: 99%

“…14,15,32,33 It has been previously described that MDSCs accumulate in peripheral lymphoid organs and migrate to tumor sites, where they contribute to immunosuppression. 15,16,33,34 Furthermore, some evidence suggests that MDSCs can induce an expansion of Tregs. 35 In addition, a transient elevation in MDSCs in mice following immunization was demonstrated.…”

Section: Studying Cd4mentioning

confidence: 99%

mRNA-based dendritic cell immunization improves survival inrettransgenic mouse melanoma model

et al. 2016

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Malignant melanoma is characterized by a rapid progression, metastasis to distant organs and resistance to chemo and radiotherapy. Although melanoma is capable of eliciting an immune response, the disease progresses and the overall results of immunotherapeutic clinical studies are not satisfactory. Recently, we have developed a novel genetic platform for improving an induction of peptide-specific CD8 C T cells by dendritic cell (DC) based on membrane-anchored b2-microglobulin (b2m) linked to a selected antigenic peptide at the N-terminus and to the cytosolic domain of TLR4 at the C-terminus. In vitro transcribed mRNA transfection of antigen-presenting cells (APCs) resulted in an efficient coupling of peptide presentation and cell activation. In this research, we utilize the chimeric platform to induce an immune response in ret transgenic mice that spontaneously develop malignant skin melanoma and to examine its effect on the overall survival of tumor-bearing mice. Following immunization with chimeric construct system, we observe a significantly prolonged survival of tumor-bearing mice as compared to the control group. Moreover, we see elevations in the frequency of CD62L hi CD44 hi central and CD62L lo CD44 hi effector memory CD8C T-cell subsets. Importantly, we do not observe any changes in frequencies of regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the vaccinated groups. Our data suggest that this novel vaccination approach could be efficiently applied for the immunotherapy of malignant melanoma.

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“…For instance, the immunosuppressive functions of myeloid-derived suppressor cells (MDSCs) critically rely on STAT3. 23,24 Mice specifically lacking STAT3 in myeloid cells are indeed more resistant than their wild-type counterparts to carcinogen-induced oncogenesis, and exhibit a superior immunological control of transplanted tumors. 25 Notably, the expression of CD274 (a potent immunosuppressive molecule also known as PD-L1) by MDSCs and other immunosuppressive myeloid cells also depends on STAT3.…”

mentioning

confidence: 99%