Relevant bibliographies by topics / Suppressive myeloid cells

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Academic literature on the topic 'Suppressive myeloid cells'

Author: Grafiati
Published: 30 November 2024

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Journal articles on the topic "Suppressive myeloid cells"

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Van Valckenborgh, Els, Jo Van Ginderachter, Kiavash Movahedi, Eline Menu, and Karin Vanderkerken. "Myeloid-Derived Suppressor Cells in Multiple Myeloma." Blood 114, no. 22 (November 20, 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 caused by an immunologically hostile microenvironment and cellular defects, such as decreased numbers of immune cells, and DC or T-cell dysfunction. However, the role of MDSCs in immune suppression in multiple myeloma is not yet described. In this study, we investigated the immunosuppressive activity and mechanism of MDSC subsets in the syngeneic and immunocompetent 5TMM mouse model (5T2 and 5T33 models). In first instance, CD11b+Ly6G− and CD11b+Ly6G+ lineage-committed myeloid MDSC subsets were detected in 5TMM-diseased bone marrow by flow cytometry. These subsets were purified via MACS from the bone marrow of naïve and 5TMM tumor-bearing mice, and analyzed for T-cell suppressive activity. Hereto, CD8+ TCR-transgenic OT-1 splenocytes were stimulated with ovalbumin protein in the presence of purified MDSC subsets, after which T-cell proliferation was measured via 3H-thymidine incorporation. Both MDSC subsets from 5TMM bone marrow were able to suppress antigen-specific T-cell responses at a higher level compared to purified MDSC subsets from normal bone marrow. On average, Ly6G− MDSCs were more suppressive than Ly6G+ MDSCs. The 5T2MM model has a tumor take of approximately 12 weeks. Three weeks after intravenous inoculation of the tumor cells, the suppressive effect of the myeloid subsets was already observed (while the plasmacytosis in the BM was very low and no detectable serum M spike was observed), indicating that T-cell suppression is an early event in MM development. To unravel the suppressive mechanism of the MDSC subsets, inhibitors were used in ovalbumin-stimulated cocultures. Ly6G− MDSC-mediated suppression was partially reversed by the iNOS inhibitor L-NMMA and the COX-2 inhibitor sc-791, both of which lower the NO concentration in culture. In contrast, superoxide dismutase and especially catalase enhance NO concentrations, resulting in enhanced T-cell suppression. None of these inhibitors had any impact on the Ly6G+ MDSC-mediated suppression. In conclusion, these data reveal the presence of MDSCs as a novel immune suppressive strategy employed by multiple myeloma cells in the bone marrow, already occurring early in the disease process. Disclosures: No relevant conflicts of interest to declare.
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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 (May 1, 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 inhibit the multitude of suppressive mechanisms employed by MDSCs. Generating tumor-reactive T cells with the capacity to resist MDSC-mediated suppression would help facilitate the production of potent anti-tumor T cell therapies. The activation of the Toll-like receptor-Myeloid differentiation factor 88 (TLR-MyD88) signaling pathway in CD8+ T cells enhances cell proliferation, cytotoxic function, and survival. Our studies show that TLR-stimulated T cells are resistant to MDSC-mediated suppression. MyD88-activated CD8+ T cells co-cultured with tumor-derived MDSCs displayed enhanced proliferation and cytokine production over control T cells. Our future objectives are to understand the molecular mechanisms by which TLR-activated T cells acquire resistance properties and to exploit this knowledge to improve antitumor immune responses by overcoming MDSC-mediated suppression.
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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 (April 1, 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 responses. HMGB1 signals through a multitude of receptors including TLR4, which is expressed by MDSC. In contrast to other inflammatory mediators which increase MDSC potency, HMGB1 reduced the suppressive capacity of TLR4(-/-) and wildtype MDSC, and reduced ROS levels in TLR4(-/-) MDSC. These findings suggest that HMGB1 may diminish MDSC function and may lead to new immunotherapeutic uses of HMGB1.
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Du, Hong, Xinchun Ding, and Cong Yan. "Metabolic reprogramming of myeloid-derived suppressive cells." Oncoscience 4, no. 3-4 (April 28, 2017): 29–30. http://dx.doi.org/10.18632/oncoscience.349.

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Oliver, Liliana, Rydell Alvarez, Raquel Diaz, Anet Valdés, Sean H. Colligan, Michael J. Nemeth, Danielle Y. F. Twum, 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 (September 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 particle’ (VSSP), attenuates MDSC function in tumor-bearing mice, which was accompanied by an increase in dendritic cells (DCs) suggesting that VSSP exhibits myeloid differentiating properties. Therefore, here, we addressed two unresolved aspects of the mechanism of action of this unique immunomodulatory agent: (1) does VSSP alter myelopoiesis in the bone marrow to redirect MDSC differentiation toward a monocyte/macrophage or DC fate? and (2) does VSSP mitigate the frequency and suppressive function of human tumor-induced MDSCs?MethodsTo address the first question, we first used a murine model of granulocyte-colony stimulating factor-driven emergency myelopoiesis following chemotherapy-induced myeloablation, which skews myeloid output toward MDSCs, especially the polymorphonuclear (PMN)-MDSC subset. Following VSSP treatment, progenitors and their myeloid progeny were analyzed by immunophenotyping and MDSC function was evaluated by suppression assays. To strengthen rigor, we validated our findings in tumor-bearing mouse models. To address the second question, we conducted a clinical trial in patients with metastatic renal cell carcinoma, wherein 15 patients were treated with VSSP. Endpoints in this study included safety and impact on PMN-MDSC frequency and function.ResultsWe demonstrated that VSSP diminished PMN-MDSCs by shunting granulocyte-monocyte progenitor differentiation toward monocytes/macrophages and DCs with heightened expression of the myeloid-dependent transcription factors interferon regulatory factor-8 and PU.1. This skewing was at the expense of expansion of granulocytic progenitors and rendered the remaining MDSCs less suppressive. Importantly, these effects were also demonstrated in a clinical setting wherein VSSP monotherapy significantly reduced circulating PMN-MDSCs, and their suppressive function.ConclusionsAltogether, these data revealed VSSP as a novel regulator of myeloid biology that mitigates MDSCs in cancer patients and reinstates a more normal myeloid phenotype that potentially favors immune activation over immune suppression.
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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 (April 6, 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 components of the neuroblastoma tumor microenvironment, suppressive myeloid cells have been described as key players in inhibition of antitumor immune responses and have been shown to positively correlate with more aggressive disease, resistance to treatments, and overall poor prognosis. This review article summarizes how neuroblastoma-driven inflammation induces suppressive myeloid cells in the tumor microenvironment and how they in turn sustain the tumor niche through suppressor functions, such as nutrient depletion and generation of oxidative stress. Numerous preclinical studies have suggested a range of drug and cellular therapy approaches to overcome myeloid-derived suppression in neuroblastoma that warrant evaluation in future clinical studies.
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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 (November 1, 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. Additional studies are needed to investigate the chemokines responsible for the tumor recruitment of CCR2+/CX3CR1+ cells and the impact of glioma derived factors on their immune suppressive phenotype. OBJECTIVE Evaluate the effect of glioma derived factors on the migration and suppression of bone marrow CCR2+/CX3CR1+ myeloid cells. METHODS A transwell migration assay was utilized to determine the migratory ability of CCR2+/CX3CR1+ cells to KR158B conditioned in the presence of CCL2 and CCL7 neutralizing antibodies. Ly6G-/GR1+ cells were isolated from bone marrow cultured with KR158B conditioned media and co-cultured with freshly isolated T-cells to examine their immune-suppressive phenotype. RESULTS KR158B gliomas differentially upregulate cytokines including CCL2, IL6, G-CSF, GM-CSF as compared to healthy naive brains. KR158B conditioned media increased the percentage of bone marrow-derived CCR2+/CX3CR1+ cells that are CD11b+, Ly6Chi, and Ly6G-. Bone marrow-derived CCR2+/CX3CR1+ cells expanded in KR158B condition media suppress both CD4+ and CD8+ T cell proliferation. Bone marrow-derived CCR2+/CX3CR1+ cells migrate to recombinant CCL2 and CCL7 as well as KR158B glioma conditioned media. Migration to conditioned media is completely inhibited by the combination of CCL2 and CCL7 neutralizing antibodies. High CCL2 and CCL7 are associated with poor prognosis in human GBM. CONCLUSION Glioma-derived CCL2 and CCL7 mediate migration of CCR2+ myeloid cells into the tumor microenvironment in a redundant manner. Additional glioma-derived factors induce CCR2+/CX3CR1+ myeloid cells to a CD4/8+ T cell suppressive state.
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Topal Gorgun, Gullu, Hiroto Ohguchi, Teru Hideshima, Yu-Tzu Tai, Noopur Raje, Nikhil C. Munshi, Paul G. Richardson, Jacob P. Laubach, and Kenneth C. Anderson. "Inhibition Of Myeloid Derived Suppressor Cells (MDSC) In The Multiple Myeloma Bone Marrow Microenvironment." Blood 122, no. 21 (November 15, 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 strategies requires not only targeting tumor or stroma cells, but also methods to overcome blockade of anti-tumor immune responses. In addition to lymphoid immune suppressor cells such as regulatory T cells (Treg), distinct populations of myeloid cells such as myeloid derived suppressor cells (MDSC) can effectively block anti-tumor immune responses, thereby representing an important obstacle for immunotherapy. While MDSC are rare or absent in healthy individuals, increased numbers of MDSC have been identified in tumor sites and peripheral circulation. We have recently assessed the presence, frequency and functional characteristics of MDSC in patients with newly diagnosed or relapsed MM compared to MM patients with response and healthy donors. We have identified an increased distinct MDSC population (CD11b+CD14-HLA-DR-/lowCD33+CD15+) with tumor promoting and immune suppressive activity in both PB and BM of MM patients. Moreover, we have shown that lenalidomide (Len) and bortezomib (Bort), either alone or in combination, do not target MDSC in MM microenvironment. Moreover, Bort-induced cytotoxicity against MM cells is abrogated in the presence of MDSCs. In solid tumors, MDSC can be targeted by treatment with the multi-targeted receptor tyrosine kinase inhibitor Sunitinib (Sun), which is therefore an effective combination agent with immunotherapy. We therefore assessed whether MDSC-mediated MM growth and immune suppression in the BM and PB can be targeted by Sun, alone or in combination with Len. We first analysed effect of Sun, alone or in combination with Len, on the tumor promoting role of MDSC versus antigen presenting cells (APC) in MM. APC (CD14+HLA-DR+), mMDSC (monocytic CD11b+CD14+HLA-DR-/lowCD33+) and nMDSCs (neutrophilic CD11b+CD14-HLA-DR-/lowCD33+CD15+) were sorted by flow cytometry from MM-BM or PB and cultured with CFSE labeled MM cell lines (MM1.S, RPMI8226 and OPM1), in the absence or presence of Sun (0.5-3uM) and Len (1uM) alone or in combination. CFSE-flow analysis demonstrated that both mMDSC and nMDSC induced MM cell proliferation compared to MM cells alone (dividing cells 51%) or cultured with APC; and importantly, that Sun significantly inhibited MM cell proliferation even in the presence of MDSC (dividing cells 28%).Importantly, Sun combined with Len further enhanced MM cell cytotoxicity in the presence of MDSC. We further analysed effect of Sun on the BM stroma (BMSC)-induced MM cell growth/proliferation. Sun alone modestly inhibited BMSC-induced MM cell growth, and Len enhanced this effect. We next evaluated Sun effect on MDSC-mediated immune suppression in MM. APC, mMDSC, nMDSC were cultured with CFSE labeled autologous CD3 T cells stimulated with CD3/CD28 for 6 days, in the presence of Sun and Len alone or in combination. CFSE flow analysis demonstrated that Sun significantly reversed MDSC-induced suppression of immune effector cells (CD4 T cells, CD8 T cells and NKT cells). Finally, we determined the effect of Sun on MDSC-associated tumor promoting and immune suppressive cytokines. Flow cytometric intracellular cytokine profiling of MDSC in MM-BM and PB demonstrated that Sun increased IFNg expression, while decreasing TNFa and IL-6 expression in MDSC. Overall our data therefore show that MDSCs are increased in the MM microenvironment and play an important role in MM pathogenesis and immune suppression. They provide the rationale for clinical evaluation of Sunitinib to inhibit the tumor-promoting and immune-suppressive functions of MDSCs and improve patient outcome in MM. Disclosures: Hideshima: Acetylon: Consultancy. Tai:Onyx: Consultancy. Munshi:Celgene: Consultancy; Novartis: Consultancy; Millennium: Consultancy. Richardson:Novartis: Consultancy; Bristol-Myers Squibb: Consultancy; Johnson & Johnson: Consultancy; Celgene: Consultancy; Millenium: Consultancy. Anderson:acetylon: Equity Ownership; oncopep: Equity Ownership; sanofi aventis: Consultancy; gilead: Consultancy; onyx: Consultancy; celgene: Consultancy.
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Petersson, Julia, Sandra Askman, Åsa Pettersson, Stina Wichert, Thomas Hellmark, Åsa C. M. Johansson, and Markus Hansson. "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. The inhibitory effect could not be explained by changed levels of mature or immature NDG in the bone marrow. Moreover, NDG isolated from the blood of both myeloma patients and healthy individuals could inhibit T-cell proliferation and IFN-γ production. On the contrary to previous studies, blood NDGs did not have to be preactivated to mediate suppressive effects. Instead, they became activated during coculture, indicating that contact with activated T-cells is important for their ability to regulate T-cells. The inhibitory effect was dependent on the production of reactive oxygen species and could be reverted by the addition of its inhibitor, catalase. Our findings suggest that blood NDGs from MM patients are suppressive, but no more than NDGs from healthy donors. However, only bone marrow NDG from MM patients exhibited MDSC function. This MDSC-like suppression mediated by bone marrow NDG could be important for the growth of malignant plasma cells in MM patients.
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D’Amico, Lucia, Sahil Mahajan, Aude-Hélène Capietto, Zhengfeng Yang, Ali Zamani, Biancamaria Ricci, David B. Bumpass, 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 (April 4, 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) targets β-catenin in MDSCs, thus exerting immune suppressive effects during tumor progression. Mice bearing extraskeletal tumors show significantly elevated levels of Dkk1 in bone microenvironment relative to tumor site. Strikingly, Dkk1 neutralization decreases tumor growth and MDSC numbers by rescuing β-catenin in these cells and restores T cell recruitment at the tumor site. Recombinant Dkk1 suppresses β-catenin target genes in MDSCs from mice and humans and anti-Dkk1 loses its antitumor effects in mice lacking β-catenin in myeloid cells or after depletion of MDSCs, demonstrating that Dkk1 directly targets MDSCs. Furthermore, we find a correlation between CD15+ myeloid cells and Dkk1 in pancreatic cancer patients. We establish a novel immunomodulatory role for Dkk1 in regulating tumor-induced immune suppression via targeting β-catenin in MDSCs.
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Dissertations / Theses on the topic "Suppressive myeloid cells"

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Benner, Brooke Nicole. "Enhancing Immunotherapy for Cancer by Targeting Suppressive Myeloid cells." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1583766367545941.

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Ortiz, Myrna Lillian. "Immature Myeloid Cells Promote Tumor Formation Via Non-Suppressive Mechanism." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5089.

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ABSTRACT Although there is ample evidence linking chronic inflammation with cancer, the cellular mechanisms involved in early events leading to tumor development remain unclear. Myeloid cells are an intricate part of inflammation. They consist of mature cells represented by macrophages, dendritic cells and granulocytes and a population of Immature Myeloid Cells (IMC), which in healthy individuals are cells in transition to mature cells. There is a substantial expansion of IMC in cancer and many other pathological conditions which is associated with pathologic activation of these cells. As a result, these cells acquire the ability to suppress immune responses and are termed Myeloid-derived Suppressor Cells (MDSCs). Although the role of MDSC in immune suppression in cancer and tumor progression is well established, their contribution to tumor development is still uncertain. The fact that cells with MDSC phenotype and function are observed in chronic inflammation raised the possibility that these cells can contribute to initial stages of tumor development. To address this question, we used an experimental system where the number of IMC was regulated by the expression of S100A9 protein. In this project, we used two different models of chronic inflammation in S100A9 transgenic (S100A9tg) and S100A9 knock-out (S100A9KO) mice. In the first model, we created the conditions for topical accumulation of these cells in the skin in the absence of infection or tissue damage using S100A9tg mice. Accumulation of IMC in the skin resulted in a dramatic increase in the formation of skin tumors during epidermal carcinogenesis. Conversely, lack of myeloid cell accumulation in S100A9KO mice substantially reduced the formation of skin papillomas. The effect of IMC was not associated with immune suppression but with the recruitment of CD4+ T cells mediated by CCL4 chemokine released by activated IMC. Elimination of CD4+ T cells or blockade of CCL4 abrogated the increase in tumor formation caused by myeloid cells. Thus, this study implicates the accumulation of IMC as an initial step in facilitating of tumor formation, which can mediate the recruitment of CD4+ T cells via the release of CCL4 chemokine. In the second model, we used inflammation-associated lung cancer caused by the chemical lung carcinogen urethane in combination with exposure to cigarette smoke referred to throughout as CS. Exposure of mice to CS alone resulted in a significant accumulation of cells with typical MDSC phenotype in different organs; however, these cells lacked immune suppressive activity and could not be defined as bona fide MDSC. When CS was combined with the single dose of urethane, it led to the accumulation of immune suppressive cells. The expansion of MDSC followed the onset of lung tumors development. This suggests that MDSC in this model is not the preceding factor but rather a consequence of tumor formation. Further studies are necessary to determine the relevance of targeting these cells for cancer treatment and prevention.
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Collazo, Ruiz Michelle Marie. "The Role of Tumor Suppressors, SHIP and Rb, in Immune Suppressive Cells." Scholar Commons, 2012. http://scholarcommons.usf.edu/etd/4016.

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Regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSC) have been extensively studied in the past 30-40 years. Their potent suppressive capacity shown in several pathological and clinical settings, such as cancer and transplantation, has made it evident that better understanding their development and function is critical. Specifically, Tregs play a pivotal role in preventing autoimmunity, graft-versus-host disease (GvHD), and organ graft rejection. We previously demonstrated that germline or induced SH2 domain-containing inositol 5-phosphatase (SHIP) deficiency in the host abrogates GvHD. Here we show that SHIP-deficiency promotes an increase of FoxP3+ cells in both the CD4+CD25+ and the CD4+CD25- T cell compartments with increased expression of Treg-associated markers. Importantly, SHIP-deficiency does not compromise Treg function. Interestingly, like conventional Tregs, SHIP-/- CD4+CD25- T cells are unresponsive to allogeneic stimulators and suppress allogeneic responses by T cells in vitro, and can mediate reduced lethal GvHD in vivo. Thus, SHIP limits the immunoregulatory capacity of CD4+ T cell, particularly in allogeneic settings. SHIP-deficiency expands the number of immunoregulatory cells in both the T lymphoid and myeloid lineages. Here, we examined if these increases are interrelated. Specifically, we found that myeloid specific SHIP-deficiency leads to expansion of both MDSC and Treg numbers. Conversely, T lineage specific ablation of SHIP leads to expansion of Treg numbers, but not expansion of MDSC, indicating an intrinsic role for SHIP in limiting Treg numbers. Interestingly, MDSC lack SHIP expression suggesting that another SHIP-deficient myeloid cell promotes MDSC and Treg expansion. Also, increased levels of G-CSF, a myelopoietic growth factor, in SHIP-/- mice may extrinsically promote MDSC expansion since we found that G-CSF is required for the expansion of splenic MDSC in mice with induced SHIP-deficiency. MDSC consist of two distinct subsets, granulocytic-MDSC (G-MDSC), and monocytic-MDSC (M-MDSC) that differ in morphology, phenotype, suppressive capacity and differentiation potential. Importantly, M-MDSC can further differentiate into dendritic cells, macrophages and preferentially into G-MDSC, in the presence of tumor-derived factors (TDF). The retinoblastoma gene (Rb1), a tumor suppressor gene and central regulator of the cell cycle and differentiation, has been shown to influence monocytic and neutrophilic lineage commitment and to limit myeloproliferative disease. Here, we examined the role of Rb1 in the biology of MDSC subsets in tumor-bearing mice. Firstly, M-MDSC expressed high levels of Rb1 which remained relatively stable in culture with GM-CSF. Conversely, freshly isolated G-MDSC initially expressed undetectable levels of Rb1 that increased over time in culture, which correlated with increased histone acetylation at the Rb1 promoter. This increased Rb1 expression and histone acetylation was accelerated by histone deacetylase inhibitors (HDACi) treatment, suggesting Rb1 expression may be controlled by histone modification. Furthermore, when treated with HDACi, M-MDSC did not differentiate into G-MDSC in culture, even with TDF present. Finally, induced Rb1 deficiency in vivo promoted an expansion of splenic CD11b+Ly6G+Ly6Clo cells, similar to G-MDSC in tumor-bearing mice. Although further studies are required, these results strongly suggest that Rb1, like SHIP, plays a role in MDSC accumulation, particularly G-MDSC in cancer.
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Zwing, Natalie [Verfasser], Falk [Akademischer Betreuer] Nimmerjahn, Falk [Gutachter] Nimmerjahn, and Gerhard [Gutachter] Krönke. "Spatial Distribution of Suppressive Myeloid Cells and Cytotoxic T Cells in Colorectal Cancer / Natalie Zwing ; Gutachter: Falk Nimmerjahn, Gerhard Krönke ; Betreuer: Falk Nimmerjahn." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2020. http://d-nb.info/123423856X/34.

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Boyer, Thomas. "Impact des cellules myéloïdes immunosuppressives dans l’induction de cellules souches cancéreuses." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0221.

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Le micro-environnement tumoral est fortement influencé par les cellules myéloïdes, dont les macrophages, les neutrophiles et les monocytes sont des représentants majeurs. Les recherches des dernières décennies ont montré que presque toutes les tumeurs sont infiltrées par des cellules myéloïdes, rendant impossible l'existence de tumeurs "froides" en ce qui concerne ces cellules. De plus, les résultats de nombreuses études cliniques se focalisant sur le compartiment immunitaire myéloïde montrent clairement que ces cellules sont presque universellement associées avec un pronostique clinique négatif chez les patients, motivant une meilleure compréhension de leur biologie et les efforts pour les cibler. Cependant, une question centrale a longtemps été de comprendre ce qui détermine les fonctions de ces cellules dans le cancer Au cours de la myélopoïèse d’urgence, l’activation pathologique des progéniteurs myéloïdes donne naissance aux cellules suppressives dérivées des myéloïdes (MDSC), une appellation rassemblant un ensemble de cellules immatures ayant une propriété commune : l’immunosuppression. En effet, les MDSC jouent un rôle crucial dans la régulation des réponses immunitaires antitumorale mais favorisent également la progression tumorale par des mécanismes non immunologiques, tels que l'influence sur l'angiogenèse et la matrice extracellulaire, la résistance aux thérapies et la préparation de la niche pré-métastatique. La préparation de la niche pré-métastatique est un élément essentiel à l’apparition de métastases à distance de la tumeur primaire, la cause principale de décès liés au cancer. Ces métastases sont initiées par une sous-population de cellules tumorales ayant des propriétés souches : les cellules souches cancéreuses (CSC). Ces cellules, aussi appelées cellules initiatrices de tumeurs (TIC), constituent une sous-population mineur au sein de la tumeur et se caractérisent par des propriétés intrinsèques distinctes telles que leur potentiel d’auto-renouvellement, la division asymétrique et leur capacité à induire une nouvelle tumeur hétérogène. D’une grande plasticité, les CSC transitionnent d’un état cellulaire à l’autre au travers de la transition épithélio-mésenchymateuse (EMT) ou son homologue, la transition mésenchymale-épithéliale (MET). De ce fait, une meilleure compréhension et des stratégies de traitements spécifiques aux CSC pourraient transformer la prise en charge clinique et améliorer significativement les taux de survie des patients. La complexité du micro-environnement tumoral, reflétée par la présence de nombreux acteurs et de leurs interactions, exerce une forte pression sélective sur les cellules cancéreuses et fournit un environnement propice à la croissance des CSC. De plus, l’implication clinique associée aux problématiques des MDSC et des CSC dirige l’émergence d’études sur leurs interactions réciproques, mais les limitations de détection de ces deux acteurs rendent l’évaluation et la compréhension des mécanismes d’interaction diffuses et incomplètes. Au cours de cette thèse, nous avons étudié le rôle des cellules myéloïdes suppressives dans l’induction de cellules cancéreuses aux propriétés souches. Nous avons montré que des cellules myéloïdes suppressives dérivées de monocyte (HuMoSC) générées in vitro, ainsi que leurs équivalents isolés de souris porteuses de tumeurs et de patients favorisaient l’apparition de CSC. Nos résultats ont mis en évidence une induction médiée par un contact direct et impliquant la forme membranaire du TGF-β. Enfin, l’étude transcriptomique des cellules myéloïdes et des cellules cancéreuses nous a également permis d’identifier une sous-population de cellules myéloïdes, exprimant la glycoprotéine CD52, comme responsable du phénomène immunosuppressif et de la plasticité des CSC vers un phénotype mésenchymateux
The tumor microenvironment is strongly influenced by myeloid cells, with macrophages, neutrophils, and monocytes being major representatives. Research over the past decades has shown that almost all tumors are infiltrated in myeloid cells, making it impossible for “cold” tumors to exist with respect to these cells. Moreover, results from numerous clinical studies focusing on the myeloid immune compartment clearly show that these cells are almost universally associated with poor clinical outcome in patients, motivating a better understanding of their biology and efforts to target them. However, a central question has long been to understand what determines the functions of these cells in cancer.During emergency myelopoiesis, pathological activation of myeloid progenitors gives rise to myeloid-derived suppressor cells (MDSC), a term that encompasses a group of immature cells with a common property: immunosuppression. Indeed, MDSC play a crucial role in regulating antitumor immune responses but also promote tumor progression through non-immunological mechanisms, such as influencing angiogenesis and the extracellular matrix, resistance to therapies, and the preparation of the pre-metastatic niche.The preparation of the pre-metastatic niche is essential for the emergence of metastases at distant sites from the primary tumor, the leading cause of cancer-related deaths. These metastases are initiated by a subpopulation of tumor cells with stem-like properties: cancer stem cells (CSC). These cells, also known as Tumor-Initiating cells (TIC), encompass a minor subpopulation within the tumor and are characterized by intrinsic properties such as self-renewal potential, asymmetric division, and the ability to induce a new, heterogeneous tumor. Highly plastic, CSC transition from one cellules state to another through the epithelial-to-mesenchymal transition (EMT) or its counterpart, the mesenchymal-to-epithelial transition (MET). Therefore, a better understanding and specific treatment strategies targeting CSC could transform clinical management and significantly improve patient survival rates.The complexity of the tumor microenvironment, reflected by the presence of numerous actors and their interactions, exerts strong selective pressure on cancer cells and provides a favorable environment for the growth of CSC. Furthermore, the clinical implications associated with the issues of MDSC and CSC drive the emergence of studies on their reciprocal interactions, but the limitations in detecting these two actors make the evaluation and understanding of their interaction mechanisms diffuse and incomplete.In this thesis, we studied the role of suppressive myeloid cells in the induction of cancer cells with stemness properties. We have shown Human Monocyte Derived Suppressive Cells (HuMoSC) generated in vitro, but also their murine and patient derived equivalent promoted the apparition of CSC. Our results have highlighted a stemness induction mediated through a direct cell-to-cell contact and involving membrane-bound TGF-β. Finally, transcriptomic study of myeloid and cancer cells allowed us to identify a subpopulation of myeloid cells, expressing the glycoprotein CD52, as responsible for the immunosuppressive properties and the plasticity of CSC towards a mesenchymal-like phenotype
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Ricchetti, Giuseppe Antonio. "An examination of the suppression of IL-10 suppression of TNF in myeloid cells." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427864.

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Ko, Jennifer S. "Mechanism of Myeloid-Derived Suppressor Cell Accumulation in Cancer and Susceptibility to Reversal by Sunitinib." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1259869673.

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Cabbage, Sarah E. "Reversible regulatory T cell-mediated suppression of myelin basic protein-specific T cells /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/5034.

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Corzo, Cesar Alexander. "Regulatory Mechanism of Myeloid Derived Suppressor Cell Activity." Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/3561.

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Myeloid-derived suppressor cells (MDSC) are a major component of the immune suppressive network that develops during cancer. MDSC down-regulate immune surveillance and antitumor immunity and facilitate tumor growth. The ability of MDSC to suppress T cell responses has been documented; however the mechanisms regulating this suppression remain to be understood. This work proposes a biological dichotomy of MDSC regulated by the tumor microenvironment. In peripheral lymphoid organs MDSC cause T-cell non-responsiveness that is antigen-specific. These MDSC have increased expression of NOX2, enabling them to produce large amounts of reactive oxygen species. Since the transcription factor STAT3 is substantially activated in MDSC, its potential role in upregulation of NOX2 expression was investigated. Over-expression of a constitutively active form of STAT3 increases expression of NOX2 subunits, whereas attenuation of STAT3 activity leads to decreased expression of NOX2. The significance of NOX2 in ROS generation is demonstrated in mice devoid of NOX2 function; NOX2- deficient MDSC are unable to inhibit antigen-induced activation of T cells. In contrast, MDSC within the tumor microenvironment have a diminished potential to generate ROS but acquire expression of arginase and inducible nitric oxide synthase, enzymes plicated in T cell non-responsiveness. Upregulation of these enzymes results in MDSC ability to inhibit lymphocyte response in absence of antigen presentation. The tumor microenvironment also promotes the differentiation of MDSC to tumor associated macrophages. Hypoxia is an exclusive feature to the tumor microenvironment and we investigated its involvement in the properties of MDSC at the tumor site. Exposure of spleen MDSC to hypoxia converts MDSC to non-specific suppressors and induces a preferential differentiation to macrophages. Stabilization of HIF-1!, a transcription factor activated by hypoxia, induces similar changes in MDCS as hypoxic exposure. Finally, ablation of HIF-1! prevents MDSC from acquiring factors that enable the suppression of T cells in absence of antigen. These findings help to expand our understanding of the biology of MDSC and suggest a regulatory pathway of myeloid cell function exclusive to the tumor microenvironment. They may also open new opportunities for therapeutic regulation as we now should take into consideration how systemic location affects the function of MDSC.
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TUMINO, NICOLA. "In HIV+ patients, Myeloid Derived Suppressor Cells induce T cell anergy by suppressing CD3ζ expression through ELF-1 inhibition." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2013. http://hdl.handle.net/2108/211078.

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The CD3ζ chain is indispensable for coupling antigen recognition to T cell response. During HIV infection, a down-modulation of CD3ζ was found on T cells, contributing to T cell anergy. It has been shown that circulating myeloid derived suppressor cells (MDSC) are elevated in HIV+ patients, and correlate with disease progression. In this work, we studied the correlation between MDSC frequency and T cell CD3ζ expression. Moreover, we investigated the mechanisms of CD3ζ decrease exploited by MDSC. CD3ζ expression and MDSC frequency were evaluated by flow cytometry on PBMC from 105 HIV+ patients. We found that granulocytic-MDSC (Gr-MDSC) were expanded in HIV+ patients compared to healthy donors; in particular, a higher Gr-MDSC frequency was observed in patients with a CD4 T cell count below 400 cells/μl. We found an inverse correlation between the percentage of Gr-MDSC and CD3ζ level. Moreover, in vitro Gr-MDSC depletion induced the up-regulation of CD3ζ in T cells, restoring the functionality of αβ, but not γδ T cells. The in vitro effect of isolated Gr-MDSC on CD3ζ expression was found cell contact-dependent, and was not mediated by previously described molecules. CD3ζ downmodulation corresponds to the decrease of its mRNA induced by silencing the transcription factor ELF-1.
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Book chapters on the topic "Suppressive myeloid cells"

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Derré, Laurent. "Myeloid-Derived Suppressive Cells in the Tumor Contexture." In Handbook of Cancer and Immunology, 1–18. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-030-80962-1_381-1.

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Papaioannou, Antonis Stylianos, Athina Boumpas, Miranta Papadopoulou, Aikaterini Hatzioannou, Themis Alissafi, and Panayotis Verginis. "Measuring Suppressive Activity and Autophagy in Myeloid-Derived Suppressor Cells." In Methods in Molecular Biology, 85–98. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-1060-2_9.

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Ma, Ge, Ping-Ying Pan, and Shu-Hsia Chen. "Myeloid-Derived Suppressive Cells and Their Regulatory Mechanisms in Cancer." In Innate Immune Regulation and Cancer Immunotherapy, 231–50. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9914-6_13.

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Bueno, Valquiria, and Graham Pawelec. "Myeloid-Derived Suppressive Cells in Ageing and Age-Related Diseases." In Healthy Ageing and Longevity, 53–64. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-87532-9_4.

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Rodríguez, Paulo C., and Augusto C. Ochoa. "Arginine Metabolism, a Major Pathway for the Suppressive Function of Myeloid-Derived Suppressor Cells." In Tumor-Induced Immune Suppression, 369–86. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8056-4_13.

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Serafini, Paolo, and Vincenzo Bronte. "Myeloid-Derived Suppressor Cells in Tumor-Induced T Cell Suppression and Tolerance." In Tumor-Induced Immune Suppression, 99–150. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8056-4_4.

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Zilio, Serena, Giacomo Desantis, Mariacristina Chioda, and Vincenzo Bronte. "Tumour-Induced Immune Suppression by Myeloid Cells." In Tumour-Associated Macrophages, 49–62. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0662-4_4.

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Vlachou, Katerina, and Panayotis Verginis. "In Vitro Suppression of CD4+ T-Cell Responses by Murine and Human Myeloid-Derived Suppressor Cells." In Methods in Molecular Biology, 119–28. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8938-6_9.

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Micouin, Anne, and Brigitte Bauvois. "Expression of Dipeptidylpeptidase IV (DPP IV/CD26) Activity on Human Myeloid and B Lineage Cells, and Cell Growth Suppression by the Inhibition of DPP IV Activity." In Advances in Experimental Medicine and Biology, 201–5. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9613-1_26.

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Ostrand-Rosenberg, Suzanne. "Immune Suppressive Myeloid-Derived Suppressor Cells in Cancer." In Encyclopedia of Immunobiology, 512–25. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-374279-7.17015-8.

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Conference papers on the topic "Suppressive myeloid cells"

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Yan, Cong, Xinchun Ding, Lingyan Wu, and Hong Du. "Abstract A12: Establishment of myeloid lineage cell line that resembles myeloid-derived suppressive cells." In Abstracts: AACR Special Conference: Metabolism and Cancer; June 7-10, 2015; Bellevue, WA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.metca15-a12.

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Marx, M., S. Troschke-Meurer, M. Zumpe, H. Lode, and N. Siebert. "Blockade of suppressive myeloid cells is effective against neuroblastoma." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687139.

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Bouchkouj, Najat, Haiying Qin, Susana Galli, John Buckley, Joanna L. Meadors, Shannon Larabee, Crystall L. Mackall, Maria G. Tsokos, and Terry J. Fry. "Abstract 1332: Pediatric sarcomas are infiltrated with myeloid derived suppressive cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1332.

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Condamine, Thomas C., Vinit Kumar, and Dmitry I. Gabrilovich. "Abstract 3176: Linking suppressive activity and ER-Stress in Myeloid Derived Suppressor Cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3176.

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Markowitz, Joseph, Taylor R. Brooks, and William E. Carson. "Abstract 3663: Immune suppressive myeloid cells expansion in vitro requires a simulated tumor microenvironment." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3663.

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Bodogai, Monica, Catalina Lee Chang, and Arya Biragyn. "Abstract 3671: Myeloid-derived suppressive cells require education from tumor-evoked Bregs to mediate metastasis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3671.

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Baugh, Aaron G., Edgar Gonzalez, Sabrina K. Zhong, Matthew B. Jacobo, Kaliya Acevedo, Jesse Kreger, Yingtong Liu, Adam L. MacLean, and Evanthia T. Roussos Torres. "874 Epigenetic modulation of myeloid derived suppressor cells decreases suppressive signaling through the STAT3 pathway." In SITC 39th Annual Meeting (SITC 2024) Abstracts, A988. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/jitc-2024-sitc2024.0874.

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Takacs, Gregory, Julia Garcia, Alexandra Sherman, Christian Kreiger, Defang Luo, and Jeffrey Harrison. "987 Glioma-derived factors induce an immune suppressive phenotype in bone marrow-derived CCR2+ myeloid cells." In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.0987.

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Markowitz, Joseph, Bonnie K. Paul, Taylor R. Brooks, Lai Wei, Jeff Pan, Katherine L. Martin, Eric Luedke, et al. "Abstract 456: Immune-suppressive myeloid cells are induced during disease progression in patients with advanced pancreatic adenocarcinoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-456.

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Hamilton, Melisa J., Momir Bosiljcic, Bryant T. Harbourne, Nancy E. LePard, Elizabeth C. Halvorsen, Ada Y. Kim, Judit P. Banath, Gerald Krystal, and Kevin L. Bennewith. "Abstract A9: Immune suppressive myeloid cells induced by hypoxic mammary tumor cells persist after primary tumor resection and promote metastatic growth." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a9.

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