Academic literature on the topic 'PMN-MDSCs'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'PMN-MDSCs.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "PMN-MDSCs"
1
Chen, Li, Li Xiong, Shubing Hong, Jin Li, Zijun Huo, Yudong Li, Shuwei Chen, et al. "Circulating Myeloid-derived Suppressor Cells Facilitate Invasion of Thyroid Cancer Cells by Repressing miR-486-3p." Journal of Clinical Endocrinology & Metabolism 105, no. 8 (June 3, 2020): 2704–18. http://dx.doi.org/10.1210/clinem/dgaa344.
Full textAbstract:
Abstract Background Myeloid-derived suppressor cells (MDSCs) have become increasingly recognized as facilitators of tumor development. However, the role of MDSCs in papillary thyroid carcinoma (PTC) progression has not been clearly explored. Objective We aimed to evaluate the levels and function of circulating MDSCs in PTC. Methods The proportion of circulating polymorphonuclear (PMN)-MDSCs and mononuclear-MDSCs from patients with PTC or benign thyroid nodules and healthy controls was measured using flow cytometry. For immunosuppressive activity analysis, sorted circulating MDSCs were cocultured with CD3/CD28-costimulated T lymphocytes and the proliferation of T cells was determined. PTC cell lines (TPC-1 and BC-PAP) were cocultured with PMN-MDSCs, and the effects on cell migration, invasion, proliferation, and apoptosis were evaluated. The differential expressed microribonucleic acids (RNAs) and messenger RNAs and their function were also explored in TPC-1 cells cocultured with or without PMN-MDSCs. Results PMN-MDSCs were increased in peripheral blood mononuclear cells of patients with PTC. Circulating PMN-MDSCs displayed strong T cell suppressive activity. PTC cells demonstrated enhanced invasive capabilities in vitro and in vivo when cocultured with sorted PMN-MDSCs. PMN-MDSCs decreased expression of miR-486-3p and activated nuclear factor kappa B2 (NF-κB2), a direct target of miR-486-3p. Rescue of miR-486-3p diminished the cell migration and invasion induced by PMN-MDSCs. Conclusion Collectively, our work indicates that circulating PMN-MDSCs promote PTC progression. By suppressing miR-486-3p, PMN-MDSCs promote the activity of the NF-κB2 signaling pathway, resulting in accelerated invasion of PTC cells, which may provide new therapeutic strategies for treatment of thyroid cancer.
2
Sprouse, Marc L., Thomas Welte, Debasish Boral, Haowen N. Liu, Wei Yin, Monika Vishnoi, Debalina Goswami-Sewell, et al. "PMN-MDSCs Enhance CTC Metastatic Properties through Reciprocal Interactions via ROS/Notch/Nodal Signaling." International Journal of Molecular Sciences 20, no. 8 (April 18, 2019): 1916. http://dx.doi.org/10.3390/ijms20081916.
Full textAbstract:
Intratumoral infiltration of myeloid-derived suppressor cells (MDSCs) is known to promote neoplastic growth by inhibiting the tumoricidal activity of T cells. However, direct interactions between patient-derived MDSCs and circulating tumors cells (CTCs) within the microenvironment of blood remain unexplored. Dissecting interplays between CTCs and circulatory MDSCs by heterotypic CTC/MDSC clustering is critical as a key mechanism to promote CTC survival and sustain the metastatic process. We characterized CTCs and polymorphonuclear-MDSCs (PMN-MDSCs) isolated in parallel from peripheral blood of metastatic melanoma and breast cancer patients by multi-parametric flow cytometry. Transplantation of both cell populations in the systemic circulation of mice revealed significantly enhanced dissemination and metastasis in mice co-injected with CTCs and PMN-MDSCs compared to mice injected with CTCs or MDSCs alone. Notably, CTC/PMN-MDSC clusters were detected in vitro and in vivo either in patients’ blood or by longitudinal monitoring of blood from animals. This was coupled with in vitro co-culturing of cell populations, demonstrating that CTCs formed physical clusters with PMN-MDSCs; and induced their pro-tumorigenic differentiation through paracrine Nodal signaling, augmenting the production of reactive oxygen species (ROS) by PMN-MDSCs. These findings were validated by detecting significantly higher Nodal and ROS levels in blood of cancer patients in the presence of naïve, heterotypic CTC/PMN-MDSC clusters. Augmented PMN-MDSC ROS upregulated Notch1 receptor expression in CTCs through the ROS-NRF2-ARE axis, thus priming CTCs to respond to ligand-mediated (Jagged1) Notch activation. Jagged1-expressing PMN-MDSCs contributed to enhanced Notch activation in CTCs by engagement of Notch1 receptor. The reciprocity of CTC/PMN-MDSC bi-directional paracrine interactions and signaling was functionally validated in inhibitor-based analyses, demonstrating that combined Nodal and ROS inhibition abrogated CTC/PMN-MDSC interactions and led to a reduction of CTC survival and proliferation. This study provides seminal evidence showing that PMN-MDSCs, additive to their immuno-suppressive roles, directly interact with CTCs and promote their dissemination and metastatic potency. Targeting CTC/PMN-MDSC heterotypic clusters and associated crosstalks can therefore represent a novel therapeutic avenue for limiting hematogenous spread of metastatic disease.
3
Tian, Xinyu, and Shengjun Wang. "LncRNA AK036396 inhibits maturation and accelerates immunosuppression of polymorphonuclear myeloid-derived suppressor cells by enhancing the stability of ficolin B." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 89.4. http://dx.doi.org/10.4049/jimmunol.204.supp.89.4.
Full textAbstract:
Abstract Long non-coding RNAs (lncRNAs) are emerging as crucial regulators of cell biology. However, the role of lncRNAs in the development and function of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) remains unclear. Here, we identified that the lncRNA AK036396 was highly expressed in PMN-MDSCs, and lncRNA AK036396 knockdown promoted the maturation and decreased the suppressive function of PMN-MDSCs. Ficolin B (Fcnb), whose expression could be used to reflect PMN-MDSC development, was the predicted target gene of lncRNA AK036396 based on microarray results. LncRNA AK036396 knockdown attenuated Fcnb protein stability in a manner dependent on the ubiquitin-proteasome system. Moreover, Fcnb inhibition downregulated the suppressive function of PMN-MDSCs. In addition, the expression of human M-ficolin, which is an orthologue of mouse Fcnb, was increased and positively correlated with arginase1 (Arg1) level in lung cancer patients. Based on these findings, lncRNA AK036396 can inhibit maturation and accelerate immunosuppression of PMN-MDSCs by enhancing Fcnb protein stability.
4
Wang, Shengjun, Xinyu Tian, Tingting Wang, Kai Yin, Dongwei Zhu, Jie Ma, and Huaxi Xu. "LncRNA AK036396/FcnB regulating polymorphonuclear myeloid-derived suppressor cells in tumor bearing mice." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 164.7. http://dx.doi.org/10.4049/jimmunol.204.supp.164.7.
Full textAbstract:
Abstract Myeloid-derived suppressor cells (MDSCs), which are constituted of immature myeloid cells, represent a population of heterogeneous cells derived from bone marrow. Activated and expanded MDSCs suppress the antitumor immune response by directly inhibiting T cell by high levels of Arg1, reactive oxygen species, and inducible nitric oxide synthase. Long non-coding RNAs (lncRNAs) are transcripts with lengths >200 nts and without the capacity to encode proteins. With the development of RNA sequencing, lncRNAs that were previously considered “transcriptional noise” have been confirmed to be involved in regulating cellular biology. However, the role of lncRNAs in the development and function of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) remains unclear. Here, we identified that the lncRNA AK036396 was highly expressed in PMN-MDSCs, and lncRNA AK036396 knockdown promoted the maturation and decreased the suppressive function of PMN-MDSCs. Ficolin B (Fcnb), whose expression could be used to reflect PMN-MDSC development, was the predicted target gene of lncRNA AK036396 based on microarray results. LncRNA AK036396 knockdown attenuated Fcnb protein stability in a manner dependent on the ubiquitin-proteasome system. Moreover, Fcnb inhibition downregulated the suppressive function of PMN-MDSCs. In addition, the expression of human M-ficolin, which is an orthologue of mouse Fcnb, was increased and positively correlated with arginase1 (Arg1) level in lung cancer patients. Based on these findings, lncRNA AK036396 can inhibit maturation and accelerate immunosuppression of PMN-MDSCs by enhancing Fcnb protein stability, which will be helpful for developing antitumor therapies targeting PMN-MDSCs.
5
Li, Xing, Xiang-yuan Wu, Nan Jiang, Yan-Fang Xing, Jie Chen, and Qu Lin. "Endoplasmic reticulum stress induced Lox-1+ CD15+ polymorphonuclear myeloid-derived suppressor cells in hepatocellular carcinoma and associated with poor prognsis." Journal of Clinical Oncology 36, no. 5_suppl (February 10, 2018): 38. http://dx.doi.org/10.1200/jco.2018.36.5_suppl.38.
Full textAbstract:
38 Background: A recent study indicated that Lectin-type oxidized LDL receptor-1 (LOX-1) was a distinct surface marker for human polymorphonuclears myeloid-derived suppressor cells (PMN-MDSC). The present study was aimed to investigate the existence LOX-1 PMN-MDSC in hepatocellular carcinoma (HCC) patients, the latent mechanism and their association with clinical parameters. Methods: 30 HCC patients and 30 health control were included. LOX-1+CD15+ PMN-MDSCs were investigated. Results: LOX-1+CD15+ PMN-MDSC were significantly elevated in both WB and PBMC of HCC patients compared with healthy control. LOX-1+CD15+ PMN-MDSC were more abundant in PBMC than WB. Addition of PMN-MDSCs resulted in significantly reduced proliferation and IFN-γ production of T cells with a dosage dependent manner. LOX-1-CD15+ PMNs present no suppressive function. The suppression on T cell proliferation and IFN-γ production was reversed by ROS inhibitor and Arginase inhibitor. ROS level of LOX-1+CD15+ PMN by DCFDA were higher in LOX-1+CD15+ PMN-MDSCs than LOX-1-CD15+ PMNs, as well as the mRNA levels of the NADPH oxidase NOX2. Meanwhile, the expression of arginase I and activity of arginase were also significantly raised in LOX-1+CD15+ PMN-MDSCs. LOX-1+CD15+ PMN-MDSCs displayed significantly higher expression of spliced X-box–binding protein 1 (sXBP1), ATF3 and CCAAT/enhancer binding protein (CHOP) were higher. For HCC patients, LOX-1+CD15+ PMN-MDSCs in WB were positively related to Cancer of the Liver Italian Program (CLIP) score. Conclusions: LOX-1+CD15+ PMN-MDSC were elevated in HCC patients and suppressed T cell proliferation through ROS/Arg I pathway with ER stress as a potential feature. LOX-1+CD15+ PMN-MDSC presented positive association with the prognosis of HCC patients.
6
Chen, Huanhuan, Keqing Yang, Lingxiao Pang, Jing Fei, Yongliang Zhu, and Jianwei Zhou. "ANKRD22 is a potential novel target for reversing the immunosuppressive effects of PMN-MDSCs in ovarian cancer." Journal for ImmunoTherapy of Cancer 11, no. 2 (February 2023): e005527. http://dx.doi.org/10.1136/jitc-2022-005527.
Full textAbstract:
BackgroundOvarian cancer is the deadliest type of malignant gynecological tumor. Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are involved ovarian cancer and are closely related to adverse outcomes. However, the immunosuppressive mechanism of PMN-MDSCs remains elusive.MethodsThe types and numbers of ANKRD22-expressing cells were investigated by bioinformatics analysis and immunohistochemical staining.Ankrd22-/-C57BL/6 mice were constructed with CRISPR-Cas9 technology. Mouse PMN-MDSCs were obtained from bone marrow (BM)-derived CD11b+Ly6G+Ly6Clowcells sorted by fluorescence-activated cell sorting with treatment of GM-CSF and IL-6, and the immunosuppressive activity of PMN-MDSCs was evaluated by flow cytometry (FCM) and ELISA. The expression level of CCR2 and the exogenous glucose uptake capacity were determined by FCM. RT-qPCR was used to detectANKRD22expression in CD11b+HLA-DR-CD14-CD15+cells from human ovarian cancer tissues, and the correlations ofANKRD22expression with the clinical characteristics and prognosis of patients were evaluated by the χ2test.ResultsWe identified a novel protein involved in regulating the immunosuppressive ability of PMN-MDSCs, ANKRD22.Ankrd22expression was high in mouse CD11b+Ly6G+Ly6Clowcells and could be significantly downregulated after exposure to a simulated microenvironmental stimulus. Knockout ofAnkrd22increased the expression level of CCR2 of CD11b+Ly6G+Ly6Clowcells and the immunosuppressive activity of PMN-MDSCs. BM-derived CD11b+Ly6G+Ly6Clowcells ofAnkrd22-/-mice significantly promoted the proliferation of ovarian cancer cells in tumor xenograft mouse models. Mechanistically, RNA sequencing showed thatWdfy1expression was obviously increased inAnkrd22-knockout BM-derived CD11b+Ly6G+Ly6Clowcells and that ectopic expression ofWdfy1increased the levels ofArg1,Inos,IdoandPdl1inAnkrd22+/+PMN-MDSCs derived from BM-derived CD11b+Ly6G+Ly6Clowcells. Surprisingly, an ANKRD22-activating candidate small-molecule compound attenuated the immunosuppressive activity ofAnkrd22+/+PMN-MDSCs. Finally, we found that lowANKRD22levels in CD11b+HLA-DR-CD14-CD15+cells derived from primary ovarian tissues were associated with a more advanced International Federation of Gynecology and Obstetrics stage, a higher recurrence rate, and a higher neutrophil-to-lymphocyte ratio.ConclusionsThese results suggest that ANKRD22 is a potential novel target for reversing the immunosuppressive effects of PMN-MDSCs.
7
Li, Xing, Qing-Jian Ye, Yan-Fang Xing, Jin-Xiang Lin, Qu Lin, and Xiang-yuan Wu. "Expansion of Lox-1+CD15+ myeloid-derived suppressor cells in hepatocellular carcinoma patients." Journal of Clinical Oncology 35, no. 7_suppl (March 1, 2017): 124. http://dx.doi.org/10.1200/jco.2017.35.7_suppl.124.
Full textAbstract:
124 Background: The top issue in the field of myeloid deprived suppressor cell (MDSC) was lack of specific markers. Lox-1 was reported to be a novel marker for polymorphonuclear MDSC (PMN-MDSC) in whole blood of head and neck cancer and lung cancer patients. The present study is aimed to detecting the lox-1 PMN-MDSC in whole blood. Methods: In the present study, a series of 24 hepatocellular carcinoma (HCC) patients and 12 healthy donors were analyzed investigating frequencies of PMN-MDSC (Lox-1+CD15+) in whole blood. The immunosuppressive function of MDSC were evaluated using T cell proliferation and activation tests. The underly mechnisms were determined using inhibitors, genes expression and activity tests. The association between MDSC and clinical parameters were determined retrospectively. Results: Patients presented significantly higher level of PMN-MDSCs. In order to confirm immune suppressive capacity of PMN-MDSCs in HCC patients, circulative PMN-MDSCs and T cells were purified using flow sorting and cocultured. T cell proliferation was abrogated by the addition of PMN-MDSC with a dosage dependent manner, as well as the production of IFN-γ. Besides, the suppression on T cell proliferation and IFN-γ production was partially reversed by reactive oxygen species (ROS) inhibitor and Arginase inhibitor. The ROS level were higher in PMN-MDSC than their normal controls. The mRNA level of NOX2, the key protein complex responsible for ROS productin in MDSC, and Arginase I were higher in PMN-MDSCs. Finally, the frequencies of PMN-MDSCs was positively associated with tumor volume. Conclusions: The present study found that Lox-1+CD15+ were novel markers for PMN-MDSCs in whole blood and very easily to be standardized between institutions.
8
Liu, Wangkai, Sitao Li, Yushan Li, Wei Shen, Haitian Chen, Xiaoyu Li, Linnuan Cai, et al. "Decreased Polymorphonuclear Myeloid-Derived Suppressor Cells and ROS Production Correlated Closely with Bronchopulmonary Dysplasia in Preterm Infants." Oxidative Medicine and Cellular Longevity 2022 (September 20, 2022): 1–8. http://dx.doi.org/10.1155/2022/9010354.
Full textAbstract:
Background. Bronchopulmonary dysplasia (BPD) is one of the most serious complications in premature infants. Myeloid-derived suppressor cells (MDSCs) have been indicated to promote immune tolerance and induce anti-inflammatory responses during the neonatal stage. However, the role of MDSCs in BPD has not been completely expounded. Methods. 130 cases of newborns were collected from six tertiary hospitals in Guangzhou from August 2019 to June 2022. They were divided into BPD group, non-BPD preterm infants group, and term infants group according to gestational age and presence of BPD. The peripheral blood was collected and used to analyze the proportion, phenotypic, and function of MDSCs at 3 to 7 days and 8 to 14 days after birth, respectively. Results. We indicated that the number of both MDSCs in premature infants is reduced, and the number of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) in peripheral blood of BPD infants was significantly lower than that of non-BPD infants under 34 weeks of gestational age ( P < 0.05 ). Furthermore, PMN-MDSCs from peripheral blood of patients presented inhibitory effect on proliferation of CD4+T and CD8+T cells in each group. However, PMN-MDSCs from BPD group had obviously weaker inhibitory effect on proliferation of CD4+T and CD8+T cells than that from non-BPD preterm infants group. In addition, we demonstrated that the expression of NADPH oxidase (Nox2) and reactive oxygen species (ROS) in PMN-MDSCs of BPD children was significantly lower than that in non-BPD preterm infants, suggesting that ROS pathway was affected in BPD in premature infants. Conclusion. This study preliminarily revealed the role of PMN-MDSCs in the pathogenesis of BPD in premature infants. The specific immune regulation mechanism of PMN-MDSCs in BPD will provide new ideas and strategies for clinical prevention and treatment of BPD in premature infants.
9
Cheng, Xiang, Hongji Zhang, Allan Tsung, and Hai Huang. "Abstract 2544: Preoperative exercise inhibits hepatic metastasis by suppressing PMN-MDSC formation of NETs." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2544. http://dx.doi.org/10.1158/1538-7445.am2022-2544.
Full textAbstract:
Abstract Introduction: Under surgical trauma, the pathological amplification and activation of neutrophils with potent immunosuppressive functions, also known as polymorphonuclear myeloid-derived suppressive cells (PMN-MDSCs), can promote metastasis by forming neutrophil extracellular traps (NETs) that are web-like structures consisting of nuclear DNA, histones, and granule proteins. Preoperative exercise (PEx) reduces postoperative complications with improved clinical outcomes in cancer patients undergoing surgeries. are. Our preliminary data show that PEx suppresses liver ischemia/reperfusion (I/R)-induced colorectal cancer (CRC) liver metastasis. Our recent studies have shown I/R-induced NETs promote liver CRC metastasis by capturing tumor cells and preventing infiltration and cytotoxicity of CD8+ T cells in tumor microenvironment (TME). We hypothesize that PEx remodels the TME by suppressing PMN-MDSCs formation of NETs. Methods: Male mice were subjected to exercise for 4 weeks, before MC38 colorectal cancer cells were injected through portal vein, and then subjected to 70% partial liver warm I/R as surgical stress. The single-cell RNA sequencing (scRNA-seq) was performed on CD45+leukocytes from TME 3 weeks after surgery. Immunofluorescence staining and Western Blot were used to determine NETs formation in the TME. Flow cytometry was used to determine the infiltration of PMN-MDSCs and CD8+ T lymphocytes in the tumors. Results: Our scRNA-seq data reveal that PEx leads to a remarkable transcriptomic shift in most immune cells types, such as PMN-MDSCs, M-MDSCs, T cells, Kupffer cells, B cells, NK and NKT cells, in the TME. PEx decreases the percentages of PMN-MDSCs in the TME and inhibits theNETs formation by PMN-MDSCs. scRNA-seq shows a significant increase of the chemokines CXCL10 in PEx-trained PMN-MDSCs obtained 3 weeks after I/R-induced hepatic metastasis, compared with sedentary controls. In addition, PEx increases the number of CD8+ T lymphocytes infiltrating the TME. Summary: Our study shows that PEx downregulates NETs formation and increases the CXCL10 expression in PMN-MDSCs, thus promoting the recruitment more cytotoxic CD8 T lymphocytes to suppress tumor metastasis. Citation Format: Xiang Cheng, Hongji Zhang, Allan Tsung, Hai Huang. Preoperative exercise inhibits hepatic metastasis by suppressing PMN-MDSC formation of NETs [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2544.
10
Bizymi, Nikoleta, Athina Damianaki, Maria Velegraki, Konstantina Zavitsanou, Anastasios Karasachinidis, Anthie Georgopoulou, Irene Mavroudi, et al. "Frequency and Functional Analysis of Myeloid-Derived Suppressor Cells (MDSCs) in the Peripheral Blood and Bone Marrow of Patients with Chronic Idiopathic Neutropenia (CIN)." Blood 136, Supplement 1 (November 5, 2020): 26–27. http://dx.doi.org/10.1182/blood-2020-136500.
Full textAbstract:
Myeloid-derived suppressor cells (MDSCs) are myeloid cells with immunoregulatory properties characterized mainly by suppression of T-cell responses (Bizymi et al, HemaSphere 2019). They are divided in HLA-DRlow/-/CD11b+/CD33+/CD15+ polymorphonuclear (PMN-MDSCs) and HLA-DRlow/-/CD11b+/CD33+/CD14+ monocytic (M-MDSCs) subsets and they are implicated in inflammatory and malignant diseases. Chronic idiopathic neutropenia (CIN), is a (usually benign) neutrophil disorder characterized by persistent and unexplained neutropenia following a detailed clinical/laboratory investigation including anti-neutrophil antibody testing, bone marrow (BM) biopsy and karyotype (Dale & Bolyard, Curr Opin Hematol 2017). Previous studies have shown that neutropenia in CIN is associated with increased apoptosis of BM granulocytic progenitor cells due to an inflammatory BM microenvironment consisting of oligoclonal T-lymphocytes, proinflammatory monocytes and proapoptotic cytokines. The aim of the present study is to explore the possible involvement of the MDSCs in the pathophysiology of CIN by investigating their number in peripheral blood (PB) and BM in association with their functional characteristics. We have studied 100 CIN patients and 49 age- and sex-matched healthy controls. The patients fulfilled the previously described diagnostic criteria for CIN (Papadaki et al, Blood 2003) and had mean neutrophil counts 1095.67 ± 479.52 (median 1215, range 100-1700). MDSC subsets were quantitated by flow cytometry in the PB mononuclear cell (PBMC) fraction using the combination of CD33PC7/CD15PC5/HLA-DRECD/CD14PE/CD11bFITC monoclonal antibodies and the Kaluza analysis software. MDSC subsets were also studied in the BMMC fraction of 24 CIN patients and 8 healthy controls from the study population. The T-cell suppression function of patient MDSCs was evaluated in coculture experiments of immunomagnetically sorted, CFSE stained, normal CD3+ cells with immunomagnetically sorted M-MDSCs and PMN-MDSCs from 4 patients and 4 healthy donors using recombinant human IL-2 as activating factor. CFSE staining was detected in the CD3+ cells on day 0 and day 3 of coculture and analysis was performed with the Fcs Express 7 software. Statistical analysis was performed with the Statistica software. We found that the proportion of PB M-MDSCs was statistically significant lower in CIN patients (1.45% ± 1.82%) compared to controls (3.68% ± 3.12%, Mann-Whitney test, p < 0.0001) (Figure a) whereas the proportion of PB PMN-MDSCs, although lower in patients, did not differ significantly from the controls. The proportion of BM M-MDSCs did not differ significantly between CIN patients and controls whereas the proportion of BM PMN-MDSCs was statistically significant lower in patients (13.27% ± 11.27%) compared to controls (19.49% ± 4.46%; Mann-Whitney test, p = 0.0291) (Figure b). Paired analysis showed that the proportion of PMN-MDSCs were higher in the BMMC compared to PBMC fraction in both CIN patients (13.27% ± 11.27% vs 1.14% ± 1.64%, respectively; Wilcoxon test, p = 0.005) (Figure c) and healthy controls (19.49% ± 4.46% vs 9.92% ± 9.08%, respectively; Wilcoxon test, p = 0.0118). Interestingly, the proportion of increase of PMN-MDSCs (in BMMC vs PBMC fraction) was significantly higher in patients (86.71% ± 21.26%) compared to controls (55.95% ± 38.59%; Mann-Whitney test, p = 0.0357) (Figure d). The above data indicate low production of PMN-MDSCs in CIN patients compared to controls but a trend for accumulation of these cells in patients' BM. No statistically significant difference was documented in paired analysis of M-MDSCs between BMMC and PBMC fractions in either CIN patients or healthy controls. Patient PMN-MDSCs and M-MDSCs displayed normal capacity to suppress T-cell proliferation as was indicated by the T-cell generations in coculture experiments of normal CD3+ cells in the presence or absence of patient MDSCs (Figure e). In conclusion, CIN patients display low proportion of MDSCs in the PB and lower proportion of PMN-MDSC in the BM compared to normal individuals. Patient MDSCs display normal capacity to suppress T-cell activation. The low proportions of MDSCs may sustain the inflammatory process associated with CIN whereas the accumulation of PMN-MDSCs in the BM represents probably a compensatory mechanism to suppress the inflammatory processes within patients' BM microenvironment. Figure Disclosures Papadaki: Genesis pharma SA: Membership on an entity's Board of Directors or advisory committees, Research Funding.
Dissertations / Theses on the topic "PMN-MDSCs"
1
Neizert, Ashley [Verfasser], and Rika [Akademischer Betreuer] Draenert. "Untersuchung der Suppressionskapazität der polymorphonuclear myeloid derived suppressor cells (PMN-MDSCs) in der chronischen HIV-1-Infektion / Ashley Neizert ; Betreuer: Rika Draenert." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1226092446/34.
Full text
2
Pettinella, Francesca. "Mature PMN-MDSCs from G-CSF-treated healthy donors and cancer patients share a suppressive gene signature and CD84 expression." Doctoral thesis, 2022. http://hdl.handle.net/11562/1067459.
Full textAbstract:
Recently, we demonstrated that neutrophil populations displaying polymorphonuclear myeloid derived suppressor cell (PMN-MDSC)-like features appear in abundance in both CD66b+ low-density neutrophils (LDNs) and normal-density neutrophils (NDNs) of healthy subjects receiving G-CSF for stem cell mobilization (GDs). We also uncovered that the mature, but not immature, fraction of PMN-MDSC populations present in GDs, similarly to what also shown by others in cancer patients, are those exerting the most potent immunosuppressive functions. Herein, by RNA-seq computational analysis, we report the identification and characterization of a distinct gene signature common to mature CD66b+CD11b+CD16+CD10+ LDNs/mNDNs from GDs (GD-mNDNs/mLDNs) and mature CD66b+CD11b+CD16+CD10+ PMN-MDSCs (mPMN-MDSCs) from head and neck (HNC) and non-small cell lung (NSCLC) cancer patients. We also show that this GD/NSCLC/HNC mPMN-MDSC gene signature derives, mostly from the maintenance of genes already expressed by normal immature neutrophil precursors, and in a minor, but more specific, quote, from genes selectively upregulated along the maturation of PMN-MDSC-committed cells. Furthermore, by searching for mRNAs included within the latter group of genes encoding surface proteins, we found CD84 expression markedly elevated on mPMN-MDSC populations, not only from GDs and HNC/NSCLC, but also from diffuse large B cell lymphoma (DLBCL), renal cell cancer (RCC), transitional cell carcinoma (TCC) and breast cancer (BC) patients. Overall, data prove that mLDNs and mNDNs from GDs represent excellent cellular models suitable either to define the molecular features, or to identify specific markers, that can be shared by mPMN-MDSC populations from different origin.
Conference papers on the topic "PMN-MDSCs"
1
Fuchs, Serge, Kevin M. Alicea-Torres, and Dmitry I. Gabrilovich. "Abstract A72: IFNAR1 signaling regulates PMN-MDSCs immune suppressive activity in cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a72.
Full text
2
Chang, Chun-Jung, Li-Chun Lu, Cher-wei Liang, Chih-Hung Hsu, and Ann-Lii Cheng. "Abstract 2067: Tumor-infiltrating PMN-MDSCs mediate sorafenib resistance in hepatocellular carcinoma through immune suppression." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2067.
Full text
3
Sprouse, Marc, Thomas Welte, Debasish Boral, Monika Vishnoi, Haowen Liu, Isabella Glitza-Oliva, and Dario Marchetti. "Abstract B23: PMN-MDSCs enhance CTC metastatic properties through reciprocal interactions via ROS/Notch/Nodal Nodal signaling." In Abstracts: AACR Special Conference on Advances in Liquid Biopsies; January 13-16, 2020; Miami, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.liqbiop20-b23.
Full text
4
Theivanthiran, Balamayooran, Nagendra Yarla, Tarek Haykal, Michael Plebanek, Y.-Van Nguyen, Nicholas DeVito, and Brent Hanks. "533 A tumor-lung NLRP3-TLR4 distant signaling axis drives immunotherapy resistance via G-CSF-dependent expansion of circulating PD1+PMN-MDSCs." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0533.
Full text