Tumor-induced Myeloid-derived Suppressor Cells

Ostrand‐Rosenberg, Suzanne; Sinha, Pratima; Beury, Daniel W.; Chornoguz, Olesya; Parker, Katherine H.

doi:10.1016/b978-0-12-394296-8.00028-2

Cited by 10 publications

(8 citation statements)

References 188 publications

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“…Starting from the early steps of cancerogenesis, tumor cells modify surrounding environment to evade host immune response (Bayne et al, 2012;Pylayeva-Gupta et al, 2012). Moreover, the recruitment to tumor mass and secondary lymphoid organs of myeloid cells with immunosuppressive activity is a prominent feature of tumor progression (Gabrilovich et al, 2012;Ostrand-Rosenberg et al, 2012;Sica and Bronte, 2007). Immature DCs, macrophages, and MDSCs are expanded and recruited by tumor-and host-released factors (Gabrilovich et al, 2012;Sica and Mantovani, 2012;Viola et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

miR-142-3p Prevents Macrophage Differentiation during Cancer-Induced Myelopoiesis

et al. 2013

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Tumor progression is accompanied by an altered myelopoiesis causing the accumulation of immunosuppressive cells. Here, we showed that miR-142-3p downregulation promoted macrophage differentiation and determined the acquisition of their immunosuppressive function in tumor. Tumor-released cytokines signaling through gp130, the common subunit of the interleukin-6 cytokine receptor family, induced the LAP∗ isoform of C/EBPβ transcription factor, promoting macrophage generation. miR-142-3p downregulated gp130 by canonical binding to its messenger RNA (mRNA) 3' UTR and repressed C/EBPβ LAP∗ by noncanonical binding to its 5' mRNA coding sequence. Enforced miR expression impaired macrophage differentiation both in vitro and in vivo. Mice constitutively expressing miR-142-3p in the bone marrow showed a marked increase in survival following immunotherapy with tumor-specific T lymphocytes. By modulating a specific miR in bone marrow precursors, we thus demonstrated the feasibility of altering tumor-induced macrophage differentiation as a potent tool to improve the efficacy of cancer immunotherapy.

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Section: Discussionmentioning

confidence: 99%

miR-142-3p Prevents Macrophage Differentiation during Cancer-Induced Myelopoiesis

et al. 2013

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“…Gr-MDSCs morphologically resemble neutrophils, however they differ from the latter in functions. In particular, Gr-MDSCs are less phagocytic, have higher activity of Arg-1 and myeloperoxidase, produce more ROS and show lower chemotaxis, e.g., toward the supernatants from human cancer cells [ 101 ]. Gr-MDSCs possess strong immunosuppressive properties, which normal PMN do not show [ 91 , 102 ].…”

Section: Gr-mdscs—the ‘Bad Guys’ In Anti-tumor Immune Responsementioning

confidence: 99%

Granulocytes and Cells of Granulocyte Origin—The Relevant Players in Colorectal Cancer

Siemińska

Poljańska

Baran

2021

IJMS

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Colorectal cancer (CRC) is one of the most common malignancy and cause of cancer death worldwide, and it still remains a therapeutic challenge for western medicine. There is strong evidence that, in addition to genetic predispositions, environmental factors have also a substantial impact in CRC development. The risk of CRC is attributed, among others to dietary habits, alcohol consumption, whereas physical activity, food containing dietary fiber, dairy products, and calcium supplements have a protective effect. Despite progress in the available therapies, surgery remains a basic treatment option for CRC. Implementation of additional methods of treatment such as chemo- and/or targeted immunotherapy, improved survival rates, however, the results are still far from satisfactory. One of the reasons may be the lack of deeper understanding of the interactions between the tumor and different types of cells, including tumor infiltrating granulocytes. While the role of neutrophils is quite well explored in many cancers, role of eosinophils and basophils is often underestimated. As part of this review, we focused on the function of different granulocyte subsets in CRC, emphasizing the beneficial role of eosinophils and basophils, as well as dichotomic mode of neutrophils action. In addition, we addressed the current knowledge on cells of granulocyte origin, specifically granulocytic myeloid derived suppressor cells (Gr-MDSCs) and their role in development and progression of CRC.

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“…Suppressive cytokines such as transforming growth factor b (TGF-b) can be co-opted by tumors to inhibit T cell function (Dahmani and Delisle, 2018;Thomas and Massagué , 2005). Tregs, myeloid-derived suppressor cells (MDSCs), and dendritic and stromal cell populations within the tumor can deprive T cells of ll necessary co-stimulatory signals or induce inhibitory signals (Chen and Mellman, 2013;Ostrand-Rosenberg et al, 2012). The excessive antigen density and kinetics of antigen exposure in solid tumors can drive exhaustion or dysfunction of T cells (Khan et al, 2019;Wherry, 2011).…”

Section: Introductionmentioning

confidence: 99%