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Journal articles on the topic 'Suppressive myeloid cells'

Author: Grafiati

Published: 30 November 2024

Last updated: 31 July 2025

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1

Van Valckenborgh, Els, Jo Van Ginderachter, Kiavash Movahedi, Eline Menu, and Karin Vanderkerken. "Myeloid-Derived Suppressor Cells in Multiple Myeloma." Blood 114, no. 22 (2009): 2794. http://dx.doi.org/10.1182/blood.v114.22.2794.2794.

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Abstract Abstract 2794 Poster Board II-770 Myeloid-derived suppressor cells (MDSCs) are a heterogeneous mix of myeloid cells in different maturation stages generated in the bone marrow. The role of MDSCs in cancer is to suppress T-cell responses, thereby likely regulating tumor progression. In mice, MDSCs are identified by the expression of the surface markers CD11b and Gr-1. Recently, Ly6G+ granulocytic (PMN-MDSC) and Ly6G− monocytic (MO-MDSC) subsets could be distinguished (Movahedi et al. Blood 2008, 111:4233-44). In multiple myeloma patients, the immune function is impaired and this is cau

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Joseph, Ann Mary, Dominique Parker, Tarik Hawkins, Nicholas Ciavattone, and Eduardo Davila. "TLR-stimulated T cells acquire resistance to MDSC mediated suppression." Journal of Immunology 198, no. 1_Supplement (2017): 205.15. http://dx.doi.org/10.4049/jimmunol.198.supp.205.15.

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Abstract The immunosuppressive tumor microenvironment presents a significant challenge to developing effective T cell-based cancer immunotherapies. Myeloid-derived suppressor cells (MDSCs), a heterogeneous group of cells, are a major contributor to the suppressive tumor microenvironment. MDSCs are immature myeloid cells that develop in response to chronic inflammation generated by an infection or a tumor. Currently, strategies to block MDSC-mediated suppression generate modest anti-tumor responses. This is in part due to lack of specific markers to target MDSCs and inability to simultaneously

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Parker, Katherine, and Suzanne Ostrand-Rosenberg. "HMGB1: a regulator of myeloid-derived suppressor cell potency? (66.37)." Journal of Immunology 186, no. 1_Supplement (2011): 66.37. http://dx.doi.org/10.4049/jimmunol.186.supp.66.37.

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Abstract Myeloid-derived suppressor cells (MDSC) are a heterogeneous population of cells that accumulate in individuals with cancer and inflammation and play a pivotal role in tumor immunity by suppressing T-cell activation and secreting proinflammatory molecules. The suppressive capacity of MDSC is mediated by immune suppressive factors such as arginase and reactive oxygen species (ROS). Nuclear protein, High Mobility Group Box1 (HMGB1), is present in nearly all cells and is released from myeloid cells as a danger response to sepsis, infection, or arthritis. Its release promotes inflammatory

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Oliver, Liliana, Rydell Alvarez, Raquel Diaz, et al. "Mitigating the prevalence and function of myeloid-derived suppressor cells by redirecting myeloid differentiation using a novel immune modulator." Journal for ImmunoTherapy of Cancer 10, no. 9 (2022): e004710. http://dx.doi.org/10.1136/jitc-2022-004710.

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BackgroundImmune suppression is common in neoplasia and a major driver is tumor-induced myeloid dysfunction. Yet, overcoming such myeloid cell defects remains an untapped strategy to reverse suppression and improve host defense. Exposure of bone marrow progenitors to heightened levels of myeloid growth factors in cancer or following certain systemic treatments promote abnormal myelopoiesis characterized by the production of myeloid-derived suppressor cells (MDSCs) and a deficiency in antigen-presenting cell function. We previously showed that a novel immune modulator, termed ‘very small size p

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Takacs, Gregory, Christian Kreiger, Defang Luo, Guimei Tian, Loic Deleyrolle, and Jeffrey Harrison. "IMMU-21. GLIOMA-DERIVED FACTORS RECRUIT AND INDUCE AN IMMUNE SUPPRESSIVE PHENOTYPE IN BONE MARROW-DERIVED CCR2+ MYELOID CELLS." Neuro-Oncology 24, Supplement_7 (2022): vii135—vii136. http://dx.doi.org/10.1093/neuonc/noac209.519.

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Abstract INTRODUCTION Infiltrating immune-suppressive myeloid cells represent a tumor supportive population that contributes to immune checkpoint inhibitor resistance and poor survival in Glioblastoma (GBM) patients. We have previously characterized monocytic-myeloid derived suppressor cells (M-MDSCs) based on their dual expression of chemokine receptors CCR2 and CX3CR1(CCR2+/CX3CR1+). Genetic and pharmacologic targeting of CCR2, in combination with PD-1 blockade, reduced the percentage of M-MDSCs in the glioma-microenvironment and slowed the progression of KR158 and 005GSC murine gliomas. Add

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Frosch, Jennifer, Ilia Leontari, and John Anderson. "Combined Effects of Myeloid Cells in the Neuroblastoma Tumor Microenvironment." Cancers 13, no. 7 (2021): 1743. http://dx.doi.org/10.3390/cancers13071743.

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Despite multimodal treatment, survival chances for high-risk neuroblastoma patients remain poor. Immunotherapeutic approaches focusing on the activation and/or modification of host immunity for eliminating tumor cells, such as chimeric antigen receptor (CAR) T cells, are currently in development, however clinical trials have failed to reproduce the preclinical results. The tumor microenvironment is emerging as a major contributor to immune suppression and tumor evasion in solid cancers and thus has to be overcome for therapies relying on a functional immune response. Among the cellular compone

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Du, Hong, Xinchun Ding, and Cong Yan. "Metabolic reprogramming of myeloid-derived suppressive cells." Oncoscience 4, no. 3-4 (2017): 29–30. http://dx.doi.org/10.18632/oncoscience.349.

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Topal Gorgun, Gullu, Hiroto Ohguchi, Teru Hideshima, et al. "Inhibition Of Myeloid Derived Suppressor Cells (MDSC) In The Multiple Myeloma Bone Marrow Microenvironment." Blood 122, no. 21 (2013): 3089. http://dx.doi.org/10.1182/blood.v122.21.3089.3089.

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Abstract The interaction of myeloma (MM) cells with bone marrow accessory cells induces genomic, epigenomic and functional changes which promote tumor development, progression, cell adhesion mediated-drug resistance (CAM-DR), and immune suppression. As in other cancers, bidirectional interaction between MM cells and surrounding cells regulates tumor development on the one hand, while transforming the BM microenvironment into a tumor promoting and immune suppressive milieu on the other. Recent developments in targeted therapies have indicated that generation of the most effective therapeutic st

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Petersson, Julia, Sandra Askman, Åsa Pettersson, et al. "Bone Marrow Neutrophils of Multiple Myeloma Patients Exhibit Myeloid-Derived Suppressor Cell Activity." Journal of Immunology Research 2021 (August 6, 2021): 1–10. http://dx.doi.org/10.1155/2021/6344344.

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Activated normal density granulocytes (NDGs) can suppress T-cell responses in a similar way as myeloid-derived suppressor cells (MDSCs). In this study, we tested the hypothesis that NDGs from blood and bone marrow of multiple myeloma (MM) patients have the ability to suppress T-cells, as MDSC. MM is an incurable plasma cell malignancy of the bone marrow. Like most malignancies, myeloma cells alter its microenvironment to promote tumor growth, including inhibition of the immune system. We found that MM NDG from the bone marrow suppressed proliferation of T-cells, in contrast to healthy donors.

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D’Amico, Lucia, Sahil Mahajan, Aude-Hélène Capietto, et al. "Dickkopf-related protein 1 (Dkk1) regulates the accumulation and function of myeloid derived suppressor cells in cancer." Journal of Experimental Medicine 213, no. 5 (2016): 827–40. http://dx.doi.org/10.1084/jem.20150950.

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Tumor–stroma interactions contribute to tumorigenesis. Tumor cells can educate the stroma at primary and distant sites to facilitate the recruitment of heterogeneous populations of immature myeloid cells, known as myeloid-derived suppressor cells (MDSCs). MDSCs suppress T cell responses and promote tumor proliferation. One outstanding question is how the local and distant stroma modulate MDSCs during tumor progression. Down-regulation of β-catenin is critical for MDSC accumulation and immune suppressive functions in mice and humans. Here, we demonstrate that stroma-derived Dickkopf-1 (Dkk1) ta

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Weichselbaum, Ralph R. "Abstract IA09: Radiotherapy immunotherapy interactions: What determines success or failure?" Clinical Cancer Research 31, no. 2_Supplement (2025): IA09. https://doi.org/10.1158/1557-3265.targetedtherap-ia09.

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Abstract Radiation therapy (RT) can both stimulate antitumor immunity and induce immunosuppressive responses, complicating its therapeutic efficacy. Data indicate that certain patient subsets—such as those undergoing combination treatment with radiation and immune-oncology drugs and/or targeted therapies may benefit from strategies that target immunosuppression or metastasis-promoting factors. One of the key challenges is the heterogeneous and context-dependent nature of myeloid suppressive states in the tumor microenvironment, which often leads to resistance to RT and immunotherapy. RT has be

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Sinha, Pratima, and Suzanne Ostrand-Rosenberg. "Withaferin A, a potent and abundant component of Withania somnifera root extract, reduces myeloid-derived suppressor cell function (P2103)." Journal of Immunology 190, no. 1_Supplement (2013): 170.8. http://dx.doi.org/10.4049/jimmunol.190.supp.170.8.

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Abstract Myeloid cells play a crucial role in growth and metastasis of malignant tumors. Tumor infiltrating myeloid cells include myeloid-derived suppressor cells (MDSC) and tumor-associated macrophages. These cells infiltrate into tumor and suppress tumor immunity by their inherent immune suppressive activity which is enhanced by interactions with each other (cross-talk). The root extract of the plant Withania somnifera (WRE) has been reported to reduce tumor cell proliferation and angiogenesis. We hypothesize that WRE or its constituents impact tumor infiltrating myeloid cells and thereby bo

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Matta, Benjamin, Brian Rosborough, Lisa Mathews, et al. "Conditional STAT3-deficiency augments Flt3 ligand-driven myeloid-derived suppressor cell expansion but limits their suppressor function (IRM7P.487)." Journal of Immunology 192, no. 1_Supplement (2014): 126.12. http://dx.doi.org/10.4049/jimmunol.192.supp.126.12.

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Abstract Fms-like tyrosine kinase 3 ligand (Flt3L) is a potent hematopoietic growth factor that profoundly expands immunostimulatory dendritic cells (DC). Despite this, the influence of Flt3L on immunoregulatory myeloid-derived suppressor cells (MDSC) has not been described. Since DC and MDSC arise from common myeloid progenitors, and Flt3L-driven DC expansion is STAT3-dependent, we sought to precisely define the role of STAT3 in MDSC downstream of Flt3L signaling. We bred myeloid cell-specific STAT3-deficient mice (LysMCre x STAT3loxP) and administered Flt3L (10 μg/d ip, 10d). Splenic DC (CD1

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Dong, Juan, Cassandra Gilmore, Hieu Ta, Keman Zhang, Sarah Stone, and Li Wang. "501 VISTA regulates the differentiation and suppressive function of myeloid-derived suppressor cells." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (2020): A536. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0501.

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BackgroundV-domain immunoglobulin suppressor of T cell activation (VISTA) is a B7 family inhibitory immune checkpoint protein and is highly expressed on myeloid cells and T cells.1 VISTA acts as both an inhibitory ligand when expressed on antigen-presenting cells and a receptor when expressed on T cells. Our recent study has shown that VISTA is a myeloid cell-specific immune checkpoint and that blocking VISTA can reprogram suppressive myeloid cells and promote a T cell-stimulatory tumor microenvironment.2 In this study, we further demonstrate that VISTA blockade directly alters the differentia

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Passioura, Toby, Alla Dolnikov, Sylvie Shen, and Geoff Symonds. "N-Ras–Induced Growth Suppression of Myeloid Cells Is Mediated by IRF-1." Cancer Research 65, no. 3 (2005): 797–804. http://dx.doi.org/10.1158/0008-5472.797.65.3.

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Abstract Activating mutations in ras oncogenes occur at high frequency in human malignancies and expression of activated ras in immortalized cells lines is generally transforming. However, somewhat paradoxically, ectopic expression of ras in some myeloid cell lines has been shown to induce growth suppression associated with up-regulation of the cyclin-dependent kinase inhibitor p21CIP1/WAF1 in a p16INK4a, p15INK4b, and p53 independent fashion. We have used cDNA array technology to compare the expression profile induced by activated N-ras (N-rasG13R) in growth-suppressed myeloid cells with that

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Filipazzi, P., R. Valenti, V. Huber, et al. "Identification of a new subset of myeloid suppressor cells in peripheral blood of melanoma patients and modulation by GM-CSF-based anti-tumor vaccine." Journal of Clinical Oncology 25, no. 18_suppl (2007): 21082. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21082.

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21082 Background: Phenotypic and functional features of myeloid suppressor cells (MSC), known to serve as critical regulators of anti-tumor T cell responses in tumor-bearing mice, are still poorly defined in human cancers. Here we analyzed myeloid subsets with suppressive activity present in peripheral blood of metastatic melanoma patients (MM) and evaluated their modulation by a GM-CSF-based anti- tumor vaccine. Methods: Stage IV AJCC MM patients (n=16) vaccinated with autologous tumor-derived heat-shock protein peptide complexes gp96 (HSPPC-96) and low dose GM-CSF provided pre- and post-trea

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Thakuri, Bal Krishna Chand, Jinyu Zhang, Juan Zhao, et al. "HCV-Associated Exosomes Upregulate RUNXOR and RUNX1 Expressions to Promote MDSC Expansion and Suppressive Functions through STAT3–miR124 Axis." Cells 9, no. 12 (2020): 2715. http://dx.doi.org/10.3390/cells9122715.

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RUNX1 overlapping RNA (RUNXOR) is a long non-coding RNA and plays a pivotal role in the differentiation of myeloid cells via targeting runt-related transcription factor 1 (RUNX1). We and others have previously reported that myeloid-derived suppressor cells (MDSCs) expand and inhibit host immune responses during chronic viral infections; however, the mechanisms responsible for MDSC differentiation and suppressive functions, in particular the role of RUNXOR–RUNX1, remain unclear. Here, we demonstrated that RUNXOR and RUNX1 expressions are significantly upregulated and associated with elevated le

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Haverkamp., Jessica, and Timothy Ratliff. "Regulatory function of myeloid-derived suppressor cells is restricted to inflammatory site. (98.25)." Journal of Immunology 184, no. 1_Supplement (2010): 98.25. http://dx.doi.org/10.4049/jimmunol.184.supp.98.25.

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Abstract Myeloid-derived suppressor cells (MDSC) are identified in mice as Gr-1+CD11b+ cells able to suppress T cell proliferation. Suppressive function of MDSC is linked to expression of arginase I and inducible nitric oxide synthase (iNOS) and can be augmented by inflammation. While inflammation is linked to MDSC function, it is unknown if MDSC isolated from the inflammatory site possess equal regulatory function as those in distal sites such as the spleen. Using the POET-3 model of prostate inflammation, we show Gr-1+CD11b+ cells isolated from inflamed prostates express elevated levels of A

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Jung, Minho, and Eun Young Choi. "TLR5 and TLR7 amplify different stage of myeloid cells." Journal of Immunology 202, no. 1_Supplement (2019): 126.40. http://dx.doi.org/10.4049/jimmunol.202.supp.126.40.

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Abstract Balance between immune activation and immune suppression is important for immune homeostasis. Toll-like receptors (TLRs) play key roles in the innate immune system, initiating inflammatory responses against pathogen infections and internal danger signals. Different TLRs recognize different kinds of ligands, but not all the TLRs do have same effect: some TLRs are immune stimulatory, while the others are immune suppressive. For instance, TLR5 ligand has been known to be immune suppressive, while TLR7 ligand has been used for immune activation. To understand how these TLR ligands lead to

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Charles, Julia, Lih-Yun Hsu, Erene Niemi, Arthur Weiss, and Mary Nakamura. "CD11blo Gr1+ osteoclast precursors are increased in inflammatory arthritis and have myeloid derived suppressor cell function. (148.1)." Journal of Immunology 186, no. 1_Supplement (2011): 148.1. http://dx.doi.org/10.4049/jimmunol.186.supp.148.1.

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Abstract We have identified a CD11blo Gr1+ bone marrow population of osteoclast precursors (OCP). This population is further defined by the markers Ly6Chi CX3CR1+ CCR2+ CD117- CD11c- and is distinct from previously characterized myeloid precursors and monocyte subsets, suggesting that osteoclasts derive from a distinct precursor analogous to the common dendritic cell precursor. OCP increase in inflammatory arthritis in mice and humans. We find that CD11blo Ly6Chi OCP increase significantly prior to the development of synovitis in zymosan-induced SKG arthritis and remain elevated throughout the

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Aykut, Berk, Ruonan Chen, Jacqueline I. Kim, et al. "Targeting Piezo1 unleashes innate immunity against cancer and infectious disease." Science Immunology 5, no. 50 (2020): eabb5168. http://dx.doi.org/10.1126/sciimmunol.abb5168.

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Piezo1 is a mechanosensitive ion channel that has gained recognition for its role in regulating diverse physiological processes. However, the influence of Piezo1 in inflammatory disease, including infection and tumor immunity, is not well studied. We postulated that Piezo1 links physical forces to immune regulation in myeloid cells. We found signal transduction via Piezo1 in myeloid cells and established this channel as the primary sensor of mechanical stress in these cells. Global inhibition of Piezo1 with a peptide inhibitor was protective against both cancer and septic shock and resulted in

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Xiong, Jia, Hui Wang, and Qingqing Wang. "Suppressive Myeloid Cells Shape the Tumor Immune Microenvironment." Advanced Biology 5, no. 3 (2021): 1900311. http://dx.doi.org/10.1002/adbi.201900311.

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Zeng, Dong, Haixia Long, and Bo Zhu. "Antitumor effects of targeting myeloid-derived suppressive cells." Translational Cancer Research 9, no. 9 (2020): 5787–97. http://dx.doi.org/10.21037/tcr.2020.01.52.

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Chen, Siqi, Yi Zhang, and Bin Zhang. "MicroRNA-155 regulates tumor myeloid-derived suppressive cells." Oncoscience 2, no. 11 (2015): 910–11. http://dx.doi.org/10.18632/oncoscience.269.

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Sica, Antonio, Laura Strauss, Francesca Maria Consonni, Cristina Travelli, Armando Genazzani, and Chiara Porta. "Metabolic regulation of suppressive myeloid cells in cancer." Cytokine & Growth Factor Reviews 35 (June 2017): 27–35. http://dx.doi.org/10.1016/j.cytogfr.2017.05.002.

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Takacs, Gregory P., Julia S. Garcia, Caitlyn A. Hodges, Christian J. Kreiger, Alexandra Sherman, and Jeffrey K. Harrison. "CSF1R Ligands Expressed by Murine Gliomas Promote M-MDSCs to Suppress CD8+ T Cells in a NOS-Dependent Manner." Cancers 16, no. 17 (2024): 3055. http://dx.doi.org/10.3390/cancers16173055.

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Glioblastoma (GBM) is the most common malignant primary brain tumor, resulting in poor survival despite aggressive therapies. GBM is characterized by a highly heterogeneous and immunosuppressive tumor microenvironment (TME) made up predominantly of infiltrating peripheral immune cells. One significant immune cell type that contributes to glioma immune evasion is a population of immunosuppressive cells, termed myeloid-derived suppressor cells (MDSCs). Previous studies suggest that a subset of myeloid cells, expressing monocytic (M)-MDSC markers and dual expression of chemokine receptors CCR2 an

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Verzoni, Elena, Monica Rodolfo, Viviana Vallacchi, et al. "Association of myeloid-derived suppressor cell (MDSC) dynamics with clinical response to nivolumab in metastatic clear cell renal carcinoma patients (mRCC): Results from the I-RENE Meet-URO 8 study." Journal of Clinical Oncology 43, no. 5_suppl (2025): 586. https://doi.org/10.1200/jco.2025.43.5_suppl.586.

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586 Background: Immune checkpoint blockade is a standard-of-care treatment for mRCC patients, but the immune mechanisms driving clinical benefit remain underexplored. In the I-RENE trial (NCT04891055), we conducted a comprehensive evaluation of myeloid-derived suppressor cell (MDSC) and lymphoid dynamics and their impact on the efficacy of nivolumab. Methods: The I-RENE study is a prospective, translational, real-world multicenter trial involving mRCC patients treated with nivolumab after failure of previous VEGFR-targeted therapies. Sixty patients were enrolled between December 2018 and Augus

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Rajan, Priyanka, Robert Zollo, Mackenzie Lieberman, et al. "Abstract 5536: The role of p38 MAPK in the tumor-induced immune suppressive microenvironment in metastatic breast cancer." Cancer Research 84, no. 6_Supplement (2024): 5536. http://dx.doi.org/10.1158/1538-7445.am2024-5536.

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Abstract The tumor microenvironment (TME) in Metastatic Breast Cancer (MBC) is a major factor contributing to therapy resistance and suppression of antitumor immune response. Tumors promote expansion and recruitment of immune suppressive cells such as myeloid-derived suppressor cells (MDSCs) contributing to tumor invasion and suppressing anti-tumor T cells. Our prior work suggested a critical role of p38 MAPK in tumor-induced expansion and mobilization of myeloid cell populations thereby facilitating metastasis. The current study examined the role of p38 MAPK in tumor-induced changes in immune

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Wieboldt, Ronja, Andreas Zingg, Emanuele Carlini, Anastasiya Börsch, Heinz Läubli, and Natalia Rodrigues Manutano. "Abstract 1259: Disturbing the Siglec-Sialoglycan axis to target myeloid- derived suppressor cells in the tumor microenvironment." Cancer Research 83, no. 7_Supplement (2023): 1259. http://dx.doi.org/10.1158/1538-7445.am2023-1259.

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Abstract Background: Overexpression of sialic acids on glycans, called hypersialylation is a common alteration in cancer that drives immune evasion via interaction with Sialic acid-binding immunoglobulin-like lectin (Siglec) immunoregulatory receptors on tumor-infiltrating immune cells. Myeloid derived suppressor cells (MDSCs) generated by cancer-induced aberrant myelopoiesis are highly immunosuppressive cells inhibiting immune cells via direct interaction or secretion of suppressive cytokines. Targeting the complex suppressive tumor microenvironment (TME) remains a challenge. Methods: Siglec

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Cornelissen, Lenneke A. M., Kim C. M. Santegoets, Esther D. Kers-Rebel, et al. "Glioma-Associated Sialoglycans Drive the Immune Suppressive Phenotype and Function of Myeloid Cells." Pharmaceutics 16, no. 7 (2024): 953. http://dx.doi.org/10.3390/pharmaceutics16070953.

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The tumor microenvironment of glioblastoma IDH-wildtype is highly immune suppressive and is characterized by a strong component of myeloid-derived suppressor cells (MDSCs). To interfere with the immune suppressive functions of MDSCs, a comprehensive understanding on how MDSCs acquire their suppressive phenotype is essential. Previously, we and others have shown a distinct Sialic acid-binding immunoglobulin-like lectin (Siglec) receptor expression profile for MDSCs in glioblastoma. Siglec receptors can transmit inhibitory signals comparable to PD-1 and are suggested to act as glyco-immune check

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Antignano, Frann, Melisa Hamilton, Carla Cohen, Victor Ho, and Gerald Krystal. "SHIP-deficient dendritic cells suppress T cell proliferation via a nitric oxide independent mechanism (91.9)." Journal of Immunology 182, no. 1_Supplement (2009): 91.9. http://dx.doi.org/10.4049/jimmunol.182.supp.91.9.

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Abstract Dendritic cells (DCs) are potent stimulators of the immune system but can also be powerful inducers of tolerance. Previous studies have shown that myeloid DC precursors are capable of suppressing T cell proliferation through a contact and nitric oxide (NO) -dependent mechanism. In addition, GM + IL-4, but not Flt3L, -derived DCs have been reported to suppress T cell proliferation by inducing T cell apoptosis. The SH2-containing inositol 5'-phosphatase (SHIP) is a potent suppressor of the PI3K pathway with known functions in regulating myeloid cell development and survival. However, li

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Rui, Ke, Jie Tian, Yue Hong, Liwei Lu, and Shengjun Wang. "Olfactory ecto-mesenchymal stem cells derived exosomes reverse the immunosuppressive capacity of myeloid-derived suppressor cells to ameliorates experimental Sjögren’s syndrome." Journal of Immunology 204, no. 1_Supplement (2020): 238.11. http://dx.doi.org/10.4049/jimmunol.204.supp.238.11.

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Abstract Primary Sjögren’s syndrome (pSS) is a systemic autoimmune disease characterized by progressive inflammation and tissue damage of salivary glands and lacrimal glands. Our previous studies have shown myeloid-derived suppressor cells (MDSCs) were significantly increased but exhibited gradually diminished suppressive capacity in experimental Sjögren’s syndrome (ESS), thus leading to the development of the disease. In this study, we found that exosomes derived from olfactory ecto-mesenchymal stem cells (OE-MSCs-Exo) effectively enhanced the suppressive function of MDSCs on T cell prolifera

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Abdelfattah, Nourhan, Parveen Kumar, Caiyi Wang, et al. "Abstract 5871: Pan-cancer myeloid cell analysis at the single cell level reveals the influence of distinct organ sites in myeloid cell phenotypes and support targeting S100A4 to reverse immune suppression." Cancer Research 83, no. 7_Supplement (2023): 5871. http://dx.doi.org/10.1158/1538-7445.am2023-5871.

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Abstract With abundant pro-tumorigenic myeloid cells and few tumoricidal tumor-infiltrating lymphocytes (&lt;5%), GBM is representative of “immune cold” tumors. As such, many different types of immunotherapies have failed to show significant benefits for most glioma patients. Hence, a better understanding of drivers of the immune suppressive microenvironment in GBM and other immune cold tumors is urgently needed to guide future immunotherapy development and application. We recently analyzed 201,986 human glioma and immune cells from 44 tissue fragments from 18 human glioma patients, and pr

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Hou, Yu, Qi Feng, Miao Xu, et al. "High-dose dexamethasone corrects impaired myeloid-derived suppressor cell function via Ets1 in immune thrombocytopenia." Blood 127, no. 12 (2016): 1587–97. http://dx.doi.org/10.1182/blood-2015-10-674531.

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Key Points The impaired suppressive function of myeloid-derived suppressor cells plays a role in the pathogenesis of immune thrombocytopenia. The effect of dexamethasone in correcting dysfunction of myeloid-derived suppressor cells suggests a new therapeutic mechanism of high-dose dexamethasone in patients with immune thrombocytopenia.

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Kumar, Vishnupriyan, Michael A. Giacomantonio, and Shashi Gujar. "Role of Myeloid Cells in Oncolytic Reovirus-Based Cancer Therapy." Viruses 13, no. 4 (2021): 654. http://dx.doi.org/10.3390/v13040654.

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Oncolytic reovirus preferentially targets and kills cancer cells via the process of oncolysis, and additionally drives clinically favorable antitumor T cell responses that form protective immunological memory against cancer relapse. This two-prong attack by reovirus on cancers constitutes the foundation of its use as an anticancer oncolytic agent. Unfortunately, the efficacy of these reovirus-driven antitumor effects is influenced by the highly suppressive tumor microenvironment (TME). In particular, the myeloid cell populations (e.g., myeloid-derived suppressive cells and tumor-associated mac

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Grewal, Eric, Leland G. Richardson, Jing Sun, et al. "493 Modulation of the Myeloid Immune Cell Microenvironment Within Gliomas by Mutant IDH." Neurosurgery 71, Supplement_1 (2025): 121. https://doi.org/10.1227/neu.0000000000003360_493.

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INTRODUCTION: Mutations in isocitrate dehydrogenase (IDH) are a significant prognostic and biological factor leading to slower growth and T cell suppression within diffuse gliomas. However, the effect of IDH and its downstream metabolites specifically on intratumoral myeloid cells remains underexplored. METHODS: Utilizing patient tumor samples, we performed RNA-sequencing and quantitative immunofluorescence on IDH-wildtype glioblastoma and IDH-mutant grade 4 astrocytoma cases. We then engineered the murine GL261 glioma cell line to harbor mutant IDH, comparing transcriptomic and cell-level cha

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Peñaloza, Hernán F., Janet S. Lee, and Prabir Ray. "Neutrophils and lymphopenia, an unknown axis in severe COVID-19 disease." PLOS Pathogens 17, no. 9 (2021): e1009850. http://dx.doi.org/10.1371/journal.ppat.1009850.

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The Coronavirus Disease 2019 (COVID-19) is caused by the betacoronavirus Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus that can mediate asymptomatic or fatal infections characterized by pneumonia, acute respiratory distress syndrome (ARDS), and multi-organ failure. Several studies have highlighted the importance of B and T lymphocytes, given that neutralizing antibodies and T cell responses are required for an effective immunity. In addition, other reports have described myeloid cells such as macrophages and monocytes play a major role in the immunity against SARS-CoV-2 as

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Parker, Katherine, and Suzanne Ostrand-Osenberg. "Title: HMGB1 both enhances and blocks myeloid-derived suppressor cell potency Katherine H. Parker, Suzanne Ostrand-Rosenberg Department of Biological Sciences, University of Maryland Baltimore County, Baltimore MD 21250 (162.40)." Journal of Immunology 188, no. 1_Supplement (2012): 162.40. http://dx.doi.org/10.4049/jimmunol.188.supp.162.40.

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Abstract Myeloid-derived suppressor cells (MDSC) are a heterogeneous population of cells that accumulate in individuals with cancer and inflammation and play a pivotal role in tumor immunity by suppressing T-cell activation and secreting proinflammatory molecules. MDSC potency is mediated by immune suppressive factors such as inducible NO synthase (iNOs), arginase, and reactive oxygen species (ROS). MDSC also impair tumor immunity through crosstalk with macrophages in which IL-10 production increases while IL-12 production decreases, causing a shift in innate and adaptive immunity towards a ty

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Anderson, Hannah, Gregory P. Takacs, Christian Kreiger, et al. "209 A CTS Team Approach to Modeling Migration and Suppression of CCR2+/CX3CR1+ Myeloid Cells in Glioblastoma." Journal of Clinical and Translational Science 6, s1 (2022): 32. http://dx.doi.org/10.1017/cts.2022.111.

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OBJECTIVES/GOALS: Evaluate the migration and immune suppressive functions of CCR2+/CX3CR1+ myeloid-derived suppressor cells (MDSCs). Integrate experimental data and biologically relevant mathematical models of infiltrating MDSCs in the context of glioblastoma (GBM). METHODS/STUDY POPULATION: CCR2+/CX3CR1+ cells were enriched from bone marrow obtained from CCR2(+/RFP)/CX3CR1(+/GFP) glioma-bearing mice to evaluate their immune-suppressive phenotype and ability to migrate to CCL2 and CCL7. Fluorescent imaging and quantification were performed on a range of tumor sizes to acquire vasculature, tumo

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Schroeder, Mark A., Julie Ritchey, Brian K. Dieckgraefe, and John F. DiPersio. "Pegylated Murine GM-CSF Increases Myeloid Derived Suppressor Cells In Vivo." Blood 118, no. 21 (2011): 2967. http://dx.doi.org/10.1182/blood.v118.21.2967.2967.

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Abstract Abstract 2967 Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of cells initially identified in tumor bearing mice that have potent immunosuppressive capabilities. Recent evidence suggests that graft-versus-host disease (GvHD) can be abrogated by ex vivo expanded, bone marrow derived, MDSCs generated in the presence of GM-CSF, G-CSF and IL-13 (Highfill et al. Blood 2010 116 :5738). It remains to be shown whether phenotypic MDSCs identified in non-tumor bearing mice are capable of immune suppression. In addition, the mechanism by which an immature myeloid cell be

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Miner, Samantha, Sawa Ito, Kazushi Tanimoto, et al. "Myeloid Leukemias Directly Suppress T Cell Proliferation Through STAT3 and Arginase Pathways." Blood 122, no. 21 (2013): 3885. http://dx.doi.org/10.1182/blood.v122.21.3885.3885.

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Abstract The immune-editing effect of myeloid leukemia has recently been reported in several studies. We previously demonstrated that the K562 leukemia-derived cell line suppresses T cell proliferation, which suggests that myeloid leukemia may function in a similar way to myeloid derived suppressor cells (MDSC). While the mechanism of suppression in leukemia is not fully understood, recent murine and human studies suggest that the STAT3 and arginase pathways play a key role in the immunosuppressive function of MDSC. We hypothesized that myeloid leukemia utilizes the MDSC STAT3 and arginase pat

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Griesinger, Andrea, Eric Prince, Andrew Donson, et al. "EPEN-22. SINGLE-CELL RNA SEQUENCING IDENTIFIES UPREGULATION OF IKZF1 IN PFA2 MYELOID SUBPOPULATION DRIVING AN ANTI-TUMOR PHENOTYPE." Neuro-Oncology 22, Supplement_3 (2020): iii312. http://dx.doi.org/10.1093/neuonc/noaa222.159.

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Abstract We have previously shown immune gene phenotype variations between posterior fossa ependymoma subgroups. PFA1 tumors chronically secrete IL-6, which pushes the infiltrating myeloid cells to an immune suppressive function. In contrast, PFA2 tumors have a more immune activated phenotype and have a better prognosis. The objective of this study was to use single-cell(sc) RNAseq to descriptively characterize the infiltrating myeloid cells. We analyzed approximately 8500 cells from 21 PFA patient samples and used advanced machine learning techniques to identify distinct myeloid and lymphoid

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Vance, Jordan K., Travis W. Rawson, Jessica M. Povroznik, Kathleen M. Brundage, and Cory M. Robinson. "Myeloid-Derived Suppressor Cells Gain Suppressive Function during Neonatal Bacterial Sepsis." International Journal of Molecular Sciences 22, no. 13 (2021): 7047. http://dx.doi.org/10.3390/ijms22137047.

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Neonates are at an increased risk of an infectious disease. This is consistent with an increased abundance of myeloid-derived suppressor cells (MDSCs) compared with older children and adults. Using a murine model of neonatal bacterial sepsis, we demonstrate that MDSCs modulate their activity during an infection to enhance immune suppressive functions. A gene expression analysis shows that MDSCs increased NOS2, Arg-1 and IL-27p28 expression in vitro and in vivo in response to Escherichia coli O1:K1:H7 and this is regulated at the level of the gene expression. Changes in the effector gene expres

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Shen, Li, and Roberto Pili. "Tasquinimod targets suppressive myeloid cells in the tumor microenvironment." OncoImmunology 8, no. 10 (2018): e1072672. http://dx.doi.org/10.1080/2162402x.2015.1072672.

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Ohayon, David E., Taylor R. Brooks, Sarah E. Mahl, Stacey A. Cranert, and Stephen N. Waggoner. "Natural killer cells support myeloid suppressor cell expansion during persistent viral infection." Journal of Immunology 198, no. 1_Supplement (2017): 78.36. http://dx.doi.org/10.4049/jimmunol.198.supp.78.36.

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Abstract Persistent viral infections in mice (e.g. lymphocytic choriomeningitis virus, LCMV) and humans (e.g. HIV, hepatitis C virus) are characterized by chronic inflammation. This sustained inflammatory milieu promotes T cell exhaustion, which limits harmful tissue damage but prevents effective viral control. We found that natural killer (NK) cells aid in the establishment of this tolerogenic state through cytolytic elimination of antiviral T cells. In parallel, others shown that chronic infection encourages expansion of immunoregulatory IL-10-expressing myeloid cells and bona fide myeloid-d

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Solito, Samantha, Erika Falisi, Claudia Marcela Diaz-Montero, et al. "A human promyelocytic-like population is responsible for the immune suppression mediated by myeloid-derived suppressor cells." Blood 118, no. 8 (2011): 2254–65. http://dx.doi.org/10.1182/blood-2010-12-325753.

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Abstract We recently demonstrated that human BM cells can be treated in vitro with defined growth factors to induce the rapid generation of myeloid-derived suppressor cells (MDSCs), hereafter defined as BM-MDSCs. Indeed, combination of G-CSF + GM-CSF led to the development of a heterogeneous mixture of immature myeloid cells ranging from myeloblasts to band cells that were able to suppress alloantigen- and mitogen-stimulated T lymphocytes. Here, we further investigate the mechanism of suppression and define the cell subset that is fully responsible for BM-MDSC–mediated immune suppression. This

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Wang, Xiang-Yang, Huanfa Yi, Chunqing Guo та Xiaofei Yu. "Myeloid-derived suppressive cells enhance differentiation of Th17 cells in an IL-1β dependent manner (P1096)". Journal of Immunology 190, № 1_Supplement (2013): 185.22. http://dx.doi.org/10.4049/jimmunol.190.supp.185.22.

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Abstract Myeloid-derived suppressive cells (MDSCs) have been implicated in the pathogenesis of several diseases, including cancer and autoimmune disorders. We found that CD11b+Gr-1+ MDSCs from tumor- or experimental autoimmune encephalomyelitis (EAE)-bearing mice promote the differentiation of naïve CD4+ T cell precursors into Th17 cells in a highly efficient manner. The presence of MDSCs also results in elevation of IL-17A production and upregulation of the orphan nuclear receptor RORA and RORC in T cells. IL-1β-derived from MDSCs is identified as a major mediator of the enhanced Th17 differ

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Good, Logan, Brooke Benner, and William E. Carson. "Bruton’s tyrosine kinase: an emerging targeted therapy in myeloid cells within the tumor microenvironment." Cancer Immunology, Immunotherapy 70, no. 9 (2021): 2439–51. http://dx.doi.org/10.1007/s00262-021-02908-5.

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AbstractBruton’s tyrosine kinase (BTK) is a non-receptor kinase belonging to the Tec family of kinases. The role of BTK in B cell receptor signaling is well defined and is known to play a key role in the proliferation and survival of malignant B cells. Moreover, BTK has been found to be expressed in cells of the myeloid lineage. BTK has been shown to contribute to a variety of cellular pathways in myeloid cells including signaling in the NLRP3 inflammasome, receptor activation of nuclear factor-κβ and inflammation, chemokine receptor activation affecting migration, and phagocytosis. Myeloid ce

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Griesinger, Andrea, Kent Riemondy, Andrew Donson, et al. "EPEN-07. SINGLE-CELL RNA SEQUENCING IDENTIFIES A UNIQUE MYELOID SUBPOPULATION ASSOCIATED WITH MESENCHYMAL TUMOR SUBPOPULATION IN POOR OUTCOME PEDIATRIC EPENDYMOMA." Neuro-Oncology 23, Supplement_1 (2021): i14—i15. http://dx.doi.org/10.1093/neuonc/noab090.057.

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Abstract We have previously shown immune gene phenotype variations between posterior fossa ependymoma subgroups. PFA1 tumors chronically secrete IL-6, which induces secretion of myeloid cell IL-8 and pushes the infiltrating myeloid cells to an immune suppressive function. In contrast, PFA2 tumors have a more immune activated phenotype associated with a better prognosis. The objective of this study was to use single-cell(sc) RNAseq to descriptively characterize the infiltrating myeloid cells. We analyzed approximately 8500 cells from 21 PFA patient samples. Using advanced machine learning, we i

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VanGundy, Zachary, Julie Baker, Heather Stranger, and Tracey Papenfuss. "Generation of mature activated regulatory myeloid cells: Differential effects of retinoic acid on myelopoiesis versus dendropoiesis (P1064)." Journal of Immunology 190, no. 1_Supplement (2013): 185.6. http://dx.doi.org/10.4049/jimmunol.190.supp.185.6.

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Abstract Myeloid cells are increasingly recognized for their potent regulatory abilities. However, factors influencing regulatory myeloid cell (regMC) differentiation remain poorly understood. Retinoic acid (RA) is a steroid hormone important in regulating mucosal (gut) immunity. RA also promotes myeloid differentiation. We hypothesize that RA during differentiation will promote regMC formation (both regulatory DCs and macrophages). Using in vitro differentiation of myeloid cells with GM-CSF with or without RA, we found that day 6-7 RA BM-MCs were more mature/activated (i.e. increased expressi

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