Relevant bibliographies by topics / MDSC

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Academic literature on the topic 'MDSC'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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Journal articles on the topic "MDSC"

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Gjerstorff, Morten F., Sofie Traynor, Odd L. Gammelgaard, Simone Johansen, Christina B. Pedersen, Henrik J. Ditzel, and Mikkel G. Terp. "PDX Models: A Versatile Tool for Studying the Role of Myeloid-Derived Suppressor Cells in Breast Cancer." Cancers 14, no. 24 (December 13, 2022): 6153. http://dx.doi.org/10.3390/cancers14246153.

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The pivotal role of myeloid-derived suppressive cells (MDSCs) in cancer has become increasingly apparent over the past few years. However, to fully understand how MDSCs can promote human tumor progression and to develop strategies to target this cell type, relevant models that closely resemble the clinical complexity of human tumors are needed. Here, we show that mouse MDSCs of both the monocytic (M-MDCS) and the granulocytic (PMN-MDSC) lineages are recruited to human breast cancer patient-derived xenograft (PDX) tumors in mice. Transcriptomic analysis of FACS-sorted MDSC-subpopulations from the PDX tumors demonstrated the expression of several MDSC genes associated with both their mobilization and immunosuppressive function, including S100A8/9, Ptgs2, Stat3, and Cxcr2, confirming the functional identity of these cells. By combining FACS analysis, RNA sequencing, and immune florescence, we show that the extent and type of MDSC infiltration depend on PDX model intrinsic factors such as the expression of chemokines involved in mobilizing and recruiting tumor-promoting MDSCs. Interestingly, MDSCs have been shown to play a prominent role in breast cancer metastasis, and in this context, we demonstrate increased recruitment of MDSCs in spontaneous PDX lung metastases compared to the corresponding primary PDX tumors. We also demonstrate that T cell-induced inflammation enhances the recruitment of MDSC in experimental breast cancer metastases. In conclusion, breast cancer PDX models represent a versatile tool for studying molecular mechanisms that drive myeloid cell recruitment to primary and metastatic tumors and facilitate the development of innovative therapeutic strategies targeting these cells.
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Smith, Alyssa D., Chunwan Lu, Daniela Payne, Amy V. Paschall, John David Klement, Priscilla S. Redd, Mohammed Ibrahim, et al. "Autocrine IL6 activates the STAT3-DNMT axis to silence the TNFa-RIP1 necroptosis pathway to sustain myeloid-derived suppressor cell survival and accumulation." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 164.10. http://dx.doi.org/10.4049/jimmunol.204.supp.164.10.

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Abstract Accumulation of myeloid-derived suppressor cells (MDSCs) is a hallmark of cancer. However, the underlying mechanism of MDSC accumulation in the tumor microenvironment (TME) remain incompletely understood. We report that MDSC accumulation is regulated by the TNFα-RIP1-mediated necroptosis. We determined that inhibition of DNMTs with Decitabine (DAC) abolished MDSC accumulation and increased activation of antigen-specific cytotoxic T lymphocytes (CTLs) in tumor-bearing mice. DAC-induced decrease of MDSC accumulation is correlated with increased IRF8 expression in MDSCs. However, DAC also abolished MDSC-like cell accumulation in IRF8 KO mice, indicating that DNA methylation does not regulate MDSC lineage differentiation but mediates MDSC accumulation at post differentiation stage. We determined that DAC decreased MDSC accumulation through increasing cell death and identified RIP1-dependent necroptosis as target of DNA methylation in MDSCs. Genome-wide DNA bisulfite sequencing revealed that the Tnf promoter is hypermethylated in tumor-induced MDSCs in vivo. Consequently, DAC dramatically increased TNFα level in MDSCs and neutralizing TNFα significantly decreased MDSC cell death. Furthermore, recombinant TNFα induced MDSC cell death in a does- and RIP1-dependent manner. IL6 which is expressed in MDSCs in tumor-bearing mice and human colorectal cancer patients. Our data shows that the autocrine IL6 activates the STAT3-DNMT axis to epigenetically silence the TNFα-RIP1 necroptosis pathway to sustain MDSC survival and accumulation in cancer. Targeting the TNFα-RIP1 necroptosis is potentially an effective approach to supress MDSCs to activate tumor-reactive CTLs in the TME.
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Aristova, T. A., E. V. Batorov, V. V. Sergeevicheva, S. A. Sizikova, G. Yu Ushakova, A. V. Gilevich, E. Ya Shevela, A. A. Ostanin, and E. R. Chernykh. "Myeloidderived peripheral blood suppressor cells at haematopoietic stem cell mobilisation in multiple myeloma patients." Russian journal of hematology and transfusiology 66, no. 2 (September 2, 2021): 218–30. http://dx.doi.org/10.35754/0234-5730-2021-66-2-218-230.

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Introduction. Multiple myeloma (MM) is a B-cell malignancy with clonal expansion of plasma cells in bone marrow. Highdose chemotherapy with autologous haematopoietic stem cell transplantation is among main consolidation therapies in MM. Myeloid-derived suppressor cells (MDSCs) are immature myeloid-accompanying cells able to suppress the immune response. The administration of granulocyte colony stimulating factor (G-CSF) to mobilise haematopoietic stem cells (HSCs) increases the MDSC count in peripheral blood (PB).Aim — to study MDSC subsets in PB of remission MM patients and their incidence dynamics at HSC mobilisation.Methods. The study surveyed 35 MM patients prior to and after HSC mobilisation. The counts of granulocytic (G-MDSCs; Lin–HLA-DR–CD33+ CD66b+), monocytic (М-MDSCs; CD14+ HLA-DRlow/–) and early MDSCs (E-MDSCs; Lin–HLA-DR– CD33+ CD66b–) were estimated in flow cytometry.Results. Remission MM patients differed from healthy donors in higher relative counts of G-MDSCs (Lin–HLA-DR– CD33+ CD66b+) and increased relative and absolute counts of М-MDSCs (CD14+ HLA-DRlow/–). М-MDSCs significantly outnumbered G-MDSCs. MDSC subset counts were elevated in complete response (CR) and very good partial response (VGPR), as well as in partial response (PR). Higher relative MDSC counts were associated with greater pretreatment (2–3 lines of chemotherapy). After HSC mobilisation with cyclophosphamide 2–4 g/m2 + G-CSF (filgrastim 5 μg/kg/day), the median relative E-MDSC and M-MDSC counts increased by 2.3 and 2.0 times, respectively, while the relative G-MDSC count raised 46-fold perturbing the MDSC subset balance.Conclusion. Remission MM patients had the increased relative G-MDSC and both relative and absolute M-MDSC counts compared to donors. A greater patient pretreatment was associated with higher relative G-MDSC counts. Treatment response (CR/VGPR vs. PR) was not coupled with MDSC count variation. The G-CSF-induced HSC mobilisation entailed a significant expansion of all three MDSC subsets in PB.
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Green, Kathy, Li Wang, Randolph Noelle, and William Green. "MDSC suppression of B cell responses in murine retrovirus-induced immunodeficiency: a role for VISTA (IRC4P.603)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 57.20. http://dx.doi.org/10.4049/jimmunol.194.supp.57.20.

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Abstract Inhibition by myeloid derived suppressor cells (MDSC) of T cell responses is well established in tumor microenvironments. We demonstrated (Green et al., 2013) induction of monocytic MDSCs during infection of B6 mice by LP-BM5 retrovirus, which causes profound immunodeficiency. These MDSCs suppressed not only T, but also B cell, responsiveness ex vivo. Whereas MDSC inhibition of stimulated T cell proliferation and IFN-gamma production was ~100%, iNOS/NO dependent, MDSC suppression of B-cell responses was only ~50% dependent on iNOS/NO - as shown by using iNOS inhibitors and iNOS k.o. mice as a source of MDSCs. We then discovered an additional mechanism(s) in MDSC inhibition of (only) B cell responsiveness that involved VISTA, a new negative checkpoint regulator. Using anti-VISTA blocking mAb, or LP-BM5 infected VISTA-/- MDSCs, MDSC inhibition of B cell responses was dependent on MDSC-expressed VISTA — again accounting for ~50% of total MDSC suppression. Combining the use of reagents to block both iNOS/NO and VISTA lead to an additive, if not synergistic, abrogation of MDSC suppression of B cell responsiveness. Consistent with a direct role of VISTA, in the absence of MDSCs, a VISTA-Ig fusion protein also partially inhibited B cell responsiveness. These results were compatible with a role for MDSC in LP-BM5-induced immunodeficiency and highlight involvement of multiple and unique suppressive pathways in the under-studied area of MDSC suppression of B cell responses.
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Xie, Qifa, Jingwen Zhang, Smita Ghare, Shirish Barve, and Craig McClain. "CD11b+/Gr-1int monocytic myeloid derived suppressor cells contribute to high-fat induced inflammation and delayed tolerance in mouse liver (54.15)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 54.15. http://dx.doi.org/10.4049/jimmunol.186.supp.54.15.

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Abstract Myeloid derived suppressor cells (MDSC) are a heterogeneous population of immature myeloid cells with universal expansion in nearly all inflammatory conditions. This study investigated the accumulation of MDSC in chronic inflammation and tolerance of obesity-related fatty liver disease. We found that the expansion of MDSC, specifically associated with the monocytic MDSC (M-MDSC): CD11b+Gr-1intLy6G-Ly6Chigh in the liver of B6 mice fed a high-fat diet contributes to liver inflammation and tolerance. M-MDSCs isolated from the liver of obese mice are more easily activated by way of Toll-like receptor (TLR4) stimulation resulting in inflammatory cytokine expression, and were functional MDSCs, readily inhibiting T cell proliferation in vitro dependent on cell-cell contact between MDSCs and T cells. The rapid accumulation of M-MDSC also contributed to delayed ConA tolerance in obesity-related fatty liver disease. M-MDSCs isolated from the liver of obese mice developed with ConA tolerance induce less liver regulatory T (Treg) cell expansion and less suppressing T cell proliferation in vitro. Experiments using mice depleted of Gr-1, or M- MDSC adoptive transfer demonstrated the important role of M-MDSC in liver inflammation and tolerance. These data unveil that M-MDSCs play an essential negative feedback function in liver immune homeostasis.
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Park, Young-Jun, Boyeong Song, Yun-Sun Kim, Eun-Kyung Kim, Jung-Mi Lee, Ga-Eun Lee, Jae-Ouk Kim, Yeon-Jeong Kim, Woo-Sung Chang, and Chang-Yuil Kang. "Myeloid derived suppressor cells(MDSCs) emergence from distinct splenic precursors (162.28)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 162.28. http://dx.doi.org/10.4049/jimmunol.188.supp.162.28.

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Abstract Myeloid derived suppressor cells(MDSCs) are a heterogenous population of immature myeloid cells, which accumulate in various pathological conditions, especially in tumor. In mice, MDSCs are characterized by the co-expression of Gr1 and CD11b molecules, and these cells could be classified into two subsets, CD11b+Ly6G+Ly6Clow polymorphonuclear neutrophil-like(PMN) MDSCs and CD11b+Ly6G-Ly6Chigh monocytic(Mo) MDSCs, by their expression of Ly6C and Ly6G molecules. Functional characteristics and fate of MDSCs are defined quite well. On the other hands, accumulation mechanism and origins of MDSC need to be more elucidated, and have not been fully understood whether MDSC could be generated in the periphery from distinct precursors in tumor microenvironment. For the first time, we identified the presence of splenic MDSC precursors in tumor bearing mice, characterized by CD11b+Ly6G-Ly6Cneg/low. We demonstrated that cytokines related to MDSC accumulation convert CD11b+Ly6G-Ly6Cneg/low cells into CD11b+Ly6G+Ly6Clow PMN-MDSC and/or CD11b+Ly6G-Ly6Chigh Mo-MDSC. These converted cells exerted strong suppressive activity on DO11.10 Tg splenocytes proliferation. Thus, these data suggest that there are peripheral distinct precursors, CD11b+Ly6Cneg/low cells, from which immunosuppressive MDSC could be generated.
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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.

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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.
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Green, Kathy A., Randolph J. Noelle, William R. Green, and Li Wang. "Checkpoint Regulator VISTA plays a role in Suppression of B-Cell Responsiveness by Monocytic Myeloid Derived Suppressor Cells from LP-BM5 retrovirus-infected Mice." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 195.14. http://dx.doi.org/10.4049/jimmunol.196.supp.195.14.

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Abstract MDSC inhibition of tumor directed T cell responses is well described. We have reported an increase of monocytic MDSC (M-MDSC) during infection of B6 mice by LP-BM5 immunodeficiency causing retrovirus. These M-MDSCs suppressed T, and B cell responsiveness ex vivo. M-MDSC inhibition of stimulated T-cell proliferation and IFN-gamma production was ~100% iNOS/NO dependent; whereas suppression of B-cells was only ~50% dependent on iNOS/NO. An additional mechanism(s) for M-MDSC inhibition of B cell responsiveness involved V-domain Ig Suppressor of T cell Activation (VISTA), negative checkpoint regulator. Using anti-VISTA blocking mAb, ~50% of total MDSC suppression of B-cell responses was dependent on MDSC-expressed VISTA. The combination of iNOS/NO inhibitors and VISTA lead to additive, if not synergistic, blockade of M-MDSC suppression of B cell responsiveness. Regarding the LP-BM5-infection dependency of M-MDSCs, spleens from uninfected mice yielded ~3-fold fewer enriched M-MDSCs; and on a per-cell basis, the M-MDSCs from uninfected mice were also substantially less suppressive (4.3 fold); than those from infected mice. Consistent with a direct role of VISTA, in the absence of M-MDSCs, a VISTA-Ig fusion protein also partially inhibited B-cell responsiveness. Initial experiments show differential VISTA expression for the LP-BM5 M-MDSC CD11b+hiLy6C+hi subpopulations we have recently defined (O’Connor et al, 2015, Virology). Thus, LP-BM5 infected, when compared to analogous subsets from uninfected mice, contain substantially more VISTA+ cells. These results suggest an unique role for M-MDSCs in LP-BM5 induced immunodeficiency, and highlight multiple suppressive pathways in the area of MDSC suppression of B cell responses.
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Green, Kathy, Li Wang, and William Green. "Suppression of B cell responsiveness by LP-BM5 retrovirus-induced myeloid derived suppressor cells generated during a murine acquired immunodeficiency syndrome: a role for negative checkpoint regulator expression on the MDSCs (VIR7P.1059)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 208.11. http://dx.doi.org/10.4049/jimmunol.192.supp.208.11.

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Abstract The inhibitory activities of myeloid derived suppressor cells (MDSC) against T cell responses are well established in tumor microenvironments. We published (2013, J. Virol. 87:2058-2071) on the induction of monocytic MDSCs during infection of susceptible B6 mice by LP-BM5 retrovirus, which causes a profound immunodeficiency. These MDSCs inhibited not only T, but also B cell, responsiveness to polyclonal stimulation in ex vivo suppression assays. Whereas MDSC inhibition of stimulated T cell proliferation and IFN-gamma production was largely iNOS/NO dependent, MDSC suppression of B cell responses was only partially (~50%) due to iNOS/NO - as shown by using iNOS inhibitors and LP-BM5 infected iNOS k.o. mice as a source of MDSCs. Here, we further study additional suppressive mechanism(s) in the MDSC inhibition of B cell responsiveness. Using MDSCs from LP-BM5 infected mice of negative checkpoint regulator knock-out origin, and specific blocking antibody, MDSC suppression of B cell responses was partly dependent on MDSC expression of certain checkpoint regulators. Combining the use of reagents to interrupt both iNOS/NO and checkpoint regulation lead to a synergistic blocking of MDSC suppression of B cell responsiveness. These results were compatible with a role for MDSC in LP-BM5 induced immunodeficiency and highlight the involvement of multiple and unique suppressive pathways in the under-studied area of MDSC suppression of B cell responses.
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Fallah, Jaleh, C. Marcela Diaz-Montero, Patricia A. Rayman, Wei (Auston) Wei, Iris Yeong Fung Sheng, James Finke, Jin Sub Kim, et al. "Correlation of myeloid-derived suppressor cells (MDSC) with pathologic complete response (pCR), recurrence free survival (RFS), and overall survival (OS) in patients with urothelial carcinoma (UC) undergoing cystectomy." Journal of Clinical Oncology 37, no. 7_suppl (March 1, 2019): 437. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.437.

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437 Background: MDSCs play an important role in maintaining a tumor immunosuppressive microenvironment. The association of circulating levels of MDSCs with pCR (pT0N0) and outcomes was investigated in patients (pts) with non-metastatic UC undergoing cystectomy. Methods: Peripheral blood samples from pts with non-metastatic UC was collected. MDSCs were measured in freshly purified peripheral blood mononuclear cells, using flow cytometry. Total (T) MDSC was defined as CD33+/HLADR-. T-MDSC subtypes were polymorphonuclear (PMN-MDSC: CD15+/CD14-), monocytic (M-MDSC: CD15-/CD14+], and uncommitted (UC-MDSC: CD15-/CD14-]. MDSC populations were presented as % of live nucleated blood cells. Wilcoxon rank sum test was used to compare MDSCs between pCR groups. Kaplan-Meier and log-rank test were used to analyze RFS and OS. Results: MDSC data were available for 124 pts (106 male, 18 female), median age 68, 28 (23%) never smokers, 93 (75%) pure UC. Thirty four pts (27%) received intravesical BCG; 49 (39%) received neoadjuvant chemotherapy (NAC); 22 (19%) had pCR (pT0N0) following surgery. PMN-MDSC was the dominant subtype (42%) and frequency of UC-MDSC and M-MDSC was 40% and 17%, respectively. Circulating levels of T-MDSC and PMN-MDSC were significantly lower in pCR patients than those in non-pCR patients (Table). Sixteen deaths were observed and 21 pts recurred after surgery. The median follow-up time of patients alive was 18.7 months (range 0.3-42.4). The median OS or RFS of all patients was not reached. One-year and two-year OS rates were 94% and 83%, respectively. One-year and two-year RFS rates were 82% and 69%, respectively. There was no association between MDSC subtypes with OS or RFS. Conclusions: Total- and PMN-MDSC subtypes in blood were significantly correlated with pCR in pts with non-metastatic UC who undergo cystectomy. The relatively short follow-up may impact the association with RFS and OS; additional follow-up is needed. [Table: see text]
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Dissertations / Theses on the topic "MDSC"

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Limagne, Emeric. "Implication des cellules myéloïdes immunosuppressives (MDSC) et des lymphocytes TH17 dans l’efficacité des chimiothérapies et de l’immunothérapie." Thesis, Paris Sciences et Lettres (ComUE), 2017. http://www.theses.fr/2017PSLEP004/document.

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L’oncologie actuelle est encore confrontée à la résistance et à la progression rapide des cancers. Les mécanismes de résistance intrinsèque développés par les cellules tumorales peuvent compromettre l’efficacité des chimiothérapies et des immunothérapies. Il est maintenant admis que l’état de la réponse immunitaire de l’hôte détermine en partie l’issue thérapeutique des patients. L’objectif de notre équipe de recherche est donc de caractériser cette réponse et d’étudier l’impact des thérapies conventionnelles sur celle-ci dans le but d’identifier les mécanismes liés à un échappement futur de la tumeur. Dans ce contexte, nous avons montré qu’une chimiothérapie (5-FU, oxaliplatine, anti-VEGF (« Vascular Endothelium Growth Factor » : FOLFOX-bevacizumab) provoque chez certains patients une chute des gMDSC (cellules myéloïdes immunosuppressives granulocytaires) périphériques qui est associée à une meilleure réponse thérapeutique. Comme chez la souris, cet effet sur les gMDSC provoque néanmoins une élévation des Th17, une population pro-angiogénique, qui limite l’efficacité de la chimiothérapie. La suite de notre travail a eu pour objectif de tester l’effet « anti-Th17 » de l’activation de l’histone désacétylase SIRT1. SIRT1 est une enzyme capable de perturber l’acétylation de STAT3, un facteur essentiel à la différenciation des Th17. Nous avons montré que l’utilisation d’agonistes pharmacologiques de SIRT1 (resvératrol, SRT1720, metformine) inhibe la polarisation des Th17 par la désacétylation de STAT3 et que cet effet permet de limiter la croissance tumorale dans un modèle de cancer colique et de mélanome chez la souris (B16F10, CT26). Nous avons validé ce concept chez l’homme, ce qui suggère qu’il est possible de cibler les Th17 par cette stratégie en complément de la chimiothérapie. Le dernier volet de ce travail est consacré à la comparaison du profil immunologique périphérique de volontaires sains à celui d’une cohorte prospective de cancers bronchiques non à petites cellules. Cette étude nous a permis de mettre en lumière les altérations immunitaires induites par la tumeur et de lier ces altérations à la réponse au nivolumab (anti-PD-1). Un premier modèle prédictif de réponse a pu être généré grâce aux données d’un panel d’analyse des cellules myéloïdes. Ce modèle révèle une fois encore que les cellules gMDSC ont un rôle prédictif défavorable, alors que les populations présentatrices d’antigènes (cellules dendritiques et monocytes) exprimant PD-L1 ont un bon rôle prédictif. Les données présentées dans cette partie sont préliminaires et devront être confirmées avec la cohorte de validation qui est en cours d’inclusion. L’ensemble de ce travail a permis de montrer qu’il est essentiel de cibler spécifiquement les cellules myéloïdes immunosuppressives et les Th17 pour favoriser l’efficacité des chimiothérapies et de l’immunothérapie dans le cancer
Actual oncology is still facing resistance and rapid progression of cancer. Intrinsic resistance mechanisms developed by tumor cells determine chemotherapy and immunotherapy efficacy. It is now recognized that the host immune response status is in part implicated in the therapeutic outcome of patients. The aim of our research team is to characterize this response and to study the impact of therapies in order to identify the mechanisms associated with future exhaust of the tumor. In this context, we have shown that chemotherapy (5-FU, oxaliplatin, anti-VEGF: FOLFOX-bevacizumab) in some patients causes a drop in devices gMDSC (granulocytic myeloid derived suppressive cells) that is associated with better therapeutic response. Nevertheless, as in mice, this effect on gMDSC causes an elevation of Th17, a pro-angiogenic population, which limits the effectiveness of chemotherapy. The result of our work was aimed to test the effect "anti-Th17" activating SIRT1 deacetylase histone. SIRT1 is an enzyme capable of disrupting the acetylation of STAT3, a key factor in the differentiation of Th17. We have shown that by using pharmacological agonists SIRT1 (resveratrol, SRT1720, metformin) inhibits Th17 polarization by deacetylation of STAT3 and that this effect can limit tumor growth in colorectal and melanoma murine models (B16F10, CT26). We validated this concept in humans, suggesting that it is possible to target Th17 cells by this strategy in addition to chemotherapy. The final component of this work is devoted to the comparison of peripheral immunological profile of healthy volunteers to a prospective cohort of non-small cell lung cancer. This study has allowed us to highlight the immune alterations induced by the tumor and to link these changes in response to nivolumab (anti-PD-1). A first response predictive model could be generated using data from a panel analysis of myeloid cells. This model proves once again that gMDSC have a negative predictive role, while antigen presenting (dendritic cells and monocytes) expressing PD-L1 has a good predictive role. Data presented in this section are preliminary and must be confirmed with the validation cohort that is currently included. All of this work has shown that it is essential to specifically target immunosuppressive myeloid cells and Th17 to promote the efficacy of chemotherapy and immunotherapy in cancer
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Metzger, Philipp [Verfasser], and Max [Akademischer Betreuer] Schnurr. "Myeloid-derived suppressor cells (MDSC) in murine pancreatic cancer: Role of IRF4 in development and function of MDSC in RIG-I-like helicase-based immunotherapy / Philipp Metzger ; Betreuer: Max Schnurr." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1213245826/34.

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Mundy-Bosse, Bethany L. "Myeloid-Derived Suppressor Cells in Tumor Immunology." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1311261626.

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Papalini, Francesca. "Analisi del programma tollerogenico delle cellule soppressorie di origine mieloide." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3423333.

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SUMMARY Tumor can activate a complex network of negative control of the immune response, inducing immunological tolerance. Antitumor chemotherapy causes immunosuppression but also favours activation of immune effectors by either triggering immunogenic cancer cell death or removing immunosoppressive constraints established in the host by growing tumors. In this work we demonstrated that the antimetabolite 5-fluoruracil can reduce for a long time the number of myeloid derived suppressor cells (MDSCs) residing in the spleen. This chemothrapeutic drug does not affect directly cancer cells but perturb a biological niche shared by central memory CD8+ T cells and a population of tumor-induced, actively proliferating, immunosuppressive myeloid cells. Depletion of this niche by surgical removal completely abrogates tumor-induced tolerance. Moreover, we began to characterize the effects of ATP on the suppressive function of MDSCs; in particularly we focused on the ATP effects mediated by P2 purinergic receptors. The preliminary data that we obtained in this study open a new prospective on a different set of metabolites that can determine the functional properties of MDSCs. This is of particular interest in cancer therapies since the extra-cellular concentration of ATP at the tumor site is abnormally elevated.
RIASSUNTO Le cellule tumorali sono in grado di modulare la reattività del sistema immunitario mediante un insieme di processi che regolano negativamente la risposta immunitaria. Questo processo è meglio noto come tolleranza immunologica. La chemioterapia antitumorale causa immunosoppressione ma favorisce anche l’attivazione di cellule effettrici del sistema immunitario sia, promuovendo la morte immunogenica delle cellule tumorali, che riducendo una componente cellulare fondamentale nella deregolazione della risposta immune indotta dal tumore. In questo lavoro abbiamo mostrato come il farmaco antimetabolita 5-fluorouracile induca un riduzione della popolazione mieloide soppressoria residente nella milza, attraverso una duratura azione che non influenza direttamente le cellule tumorali e che dipende integralmente dalla perturbazione della nicchia biologica condivisa dalle cellule CD8+ T central memory (TCM) e da un popolazione di cellule mieloidi attivate dal tumore, altamente proliferanti e dotate di una potente azione immunosoppressiva. L’eliminazione di questa nicchia mediante rimozione chirurgica della milza abroga completamente la tolleranza immunitaria indotta dal tumore. Inoltre, allo scopo di studiare i complessi meccanismi molecolari responsabili della funzione soppressoria delle MDSC, abbiamo caratterizzato la risposta purinergica P2-mediata indotta da ATP nelle cellule mieloidi, gettando le basi per una futura e approfondita indagine degli effetti mediati da questo messaggero extracellulare presente in elevate concentrazioni nel microambiente tumorale.
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Assimacopoulos, Evangelia Maria. "Monitoring and Targeting of Myeloid-Derived Suppressor Cells (MDSC) in Different Mouse Cancer Models." Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/318817.

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Lereclus, Emilie. "Origine et rôles des cellules myéloïdes suppressives dans le sepsis." Thesis, Limoges, 2018. http://www.theses.fr/2018LIMO0060/document.

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Les Myeloid-Derived Suppressor Cells (MDSC) sont une population hétérogène de cellules myéloïdes immatures, regroupées en deux sous-populations : les monocytiques-MDSC (M-MDSC) et les polymorphonucléaires-MDSC (PMN-MDSC). Ces cellules ont des capacités immunosuppressives et peuvent exprimer le ligand PD-L1 induisant l’anergie des lymphocytes T qui expriment le marqueur PD-1. Au cours du sepsis, divers bouleversements immunologiques surviennent, et la fonction majeure des MDSC est probablement de réguler l’hyper-inflammation en participant à l’état d’immunodépression rencontré chez les patients. Ceux-ci ont alors un risque de développer des infections secondaires, et de réactiver des virus jusque-là en latence. Notre étude a pour objectifs de mettre en évidence l’origine des MDSC dans le sepsis, et d’approfondir leurs rôles dans l’état d’immunosuppression, notamment dans la réactivation du Torque Teno Virus (TTV). Nos résultats montrent tant ex vivo qu’in vitro, que dans le sepsis, les MDSC sont produites par la moelle osseuse, sous l’influence du G-CSF et de l’IL-6. Ces cellules exprimant PD-L1, sont augmentées dans le sang très tôt dans le sepsis et persistes au cours de l’hospitalisation. L’augmentation de la charge virale du TTV est observée dans le sang périphérique des patients, mais n’est pas corrélée à la fréquence des MDSC. Ces résultats suggèrent que lors d’un sepsis, l’orage cytokinique stimule la production de MDSC exprimant PD-L1 par la moelle osseuse, qui une fois en périphérie, vont participer à l’immunosuppression générale
Myeloid-Derived Suppressor Cells (MDSC) are a heterogeneous population of immature myeloid cell, and are regrouped in two subsets: the monocytic-MDSC (M-MDSC) and the polymorphonuclear-MDSC (PMN-MDSC). These cells have immunosuppressive capacities and mainly act on T cells. MDSC can express the ligand PD-L1 and induce PD-1 expressing-T cells exhaustion. During sepsis, several immunological changes occur, and MDSC probably downregulate the hyper-inflammatory state, contributing to the immunosuppression phase encountered in patients after a sepsis. Immunocompromised patients can develop secondary infections, and reactivate latent virus. The aims of our study were to highlight the origin of MDSC in sepsis, and to explore their roles in the immunosuppression state, especially in the Torque Teno Virus (TTV) reactivation. Our results show, both ex vivo and in vitro, that in sepsis, MDSC originate from bone marrow are induced by G-CSF and IL-6. These PD-L1 expressing-cells are increased in peripheral blood very early in sepsis, and persist during hospitalization. These MDSC are able to inhibit T cells in vitro. The increase of TTV viral load is observed in peripheral blood of patients but is not correlated with MDSC frequencies. These results suggest that during sepsis, the cytokine storm boosts PD-L1 expressing MDSC’s production by bone marrow, which contribute in peripheral blood to the immunosuppression
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Falisi, Erika. "Caratterizzazione di una sottopopolazione mieloide umana analoga ai promielociti e dotata di attività immunosoppressoria." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3421993.

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The ability of the immune system to avoid self-reactivity and autoimmune diseases is achieved by central and peripheral tolerance. Immune tolerance is susteined by different population, one of which is represented by myeloid-derived suppressor cells (MDSC). MDSC are a heterogeneous population of cells consisting of myeloid progenitor cells and immature myeloid cells that are able to suppress both adaptative and innate immunity. In pathological conditions, such as cancer, various infectious diseases and autoimmune diseases, the release of soluble factors induce the increase of myelopoiesis and a partial block of the maturation of myeloid cells. These soluble factors are also believed to be involved in the mobilization and activation of MDSC. MDSC was found in tumour-bearing mice but also in cancer patients. While the phenotype of murine MDSC is well defined by specific markers, like Gr-1, CD11b e IL4Rα, the immunophenotype of human MDSC is still not well defined. In recent years, both in tumour-bearing mice and in cancer patients, MDSC was identified with granulocytes or monocytes features. In this work we demonstrated that human MDSC can be induced in vitro by cytokine treatment of myeloid progenitors. Our data show that the combination of G-CSF and GM-CSF induce the accumulation of immature myeloid cells (BM-MDSC) with features resembling those we identified in the blood of cancer patients. We also demonstrated that BM-MDSC are able to suppress T cells proliferation and that this suppression is accompanied by the downregulation of CD3ζ and CD3ε chains and by the reduction of IFN-γ secreted by activated lymphocyte. Since BM-MDSCs consist of a heterogeneous population, we focused our research to identify the subpopulation of BM-MDSC characterized by the suppressive activity. We demonstrated that human MDSC are immature cells blocked in a particular stage of differentiation. This cells, identifided by the phenotype CD16-/CD11blow/-, showed morphological features of ex-vivo-bone marrow isolated promyelocytes but, unlike these, they are smaller, less grainy, and are able to suppress T lymphocyte proliferation also by CD3ε downregulation. We also observed that the suppressive subpopulation is composed by other two fractions that distinguish each other by a different emission in the red wavelenght, a different grain and a different ability to suppress T lymphocyte proliferation. In the second section of this work we focused in the evaluation of chemotherapy on the accumulation and the functionality of MDSC, one of the main population involved in tumor immunosuppression and in the failure of immunotherapy. Our data showed that, in analogy to the results obtained in mice, 5-fluorouracil is able to remove the suppressive effect of BM-MDSCs on T lymphocyte proliferation. These observation allow us to suggest the use of chemotherapy like adiuvant in immunotherapy approaches.
Il sistema immunitario è in grado di bloccare il riconoscimento degli antigeni self e quindi lo sviluppo di risposte autoimmunitarie mediante il mantenimento della tolleranza immunitaria. Tale fenomeno viene sostenuto dall’azione di diverse popolazioni cellulari tolerogeniche, una delle quali è rappresentata cellule soppressorie di derivazione mieloide (MDSC). Le MDSC sono una popolazione molto eterogenea composta da cellule mieloidi immature caratterizzate dalla capacità di sopprimere sia la risposta immunitaria innata che quella adattativa. È stato ipotizzato che in condizioni patologiche, quali infezioni, malattie autoimmunitarie e neoplasie, il rilascio di diversi fattori di crescita induca l’aumento della mielopoiesi ed il blocco maturativo delle cellule mieloidi che si accumulano in uno stato di immaturità. Tali fattori solubili sono inoltre ritenuti coinvolti nella mobilizzazione e nell’attivazione delle MDSC. Le MDSC sono state identificate sia nel modello murino che in pazienti affetti da tumore. Mentre il fenotipo delle MDSC murine è facilmente identificabile mediante l’uso di marcatori specifici (Gr-1, CD11b e IL4Rα), le caratteristiche immunofenotipiche delle MDSC umane non sono ancora state definite. Nonostante questo, sia nel modello murino che nei pazienti affetti da tumore, le MDSC si sono dimostrate avere caratteristiche talvolta granulocitarie e talvolta monocitarie. In questo lavoro abbiamo dimostrato che è possibile indurre, in vitro, la generazione di MDSC umane a partire da precursori midollari coltivati in presenza di diversi fattori solubili, tra i quali il G-CSF ed il GM-CSF. Il nostro studio ha dimostrato che l’uso combinato di G-CSF e di GM-CSF permette di indurre l’accumulo di cellule mieloidi immature (BM-MDSC) con caratteristiche simili a quelle da noi identificate nel sangue di pazienti affetti da tumore. Le BM-MDSC sono in grado di inibire la proliferazione di linfociti T attivati sia con mitogeni che con allo-antigeni. Inoltre abbiamo dimostrato che la soppressione mediata dalle BM-MDSC è associata sia alla diminuzione dell’espressione delle catene ζ ed ε del CD3 che alla riduzione della produzione di IFN-γ secreto dagli stessi linfociti T. Considerando l’elevata eterogeneità delle BM-MDSC, in questo lavoro abbiamo cercato di identificare quali sottopopolazioni di BM-MDSC fossero responsabili dall’attività soppressoria. Mediante esperimenti di sorting cellulare abbiamo dimostrato, che le BM-MDSC sono cellule immature ascrivibili ad un preciso stadio di differenziazione. Queste cellule, definite dal fenotipo CD16-/CD11blow/-, presentano infatti caratteristiche morfologiche simili ai promielociti isolati dal midollo ex-vivo ma, a differenza di queste, sono caratterizzate da una minore granulosità, da maggiori dimensioni e dalla capacità si sopprimere la proliferazione linfocitaria accompagnata anche dalla diminuzione dell’espressione della catena ε del CD3 espressa sulla superficie dei linfociti T. Abbiamo inoltre evidenziato l’eterogeneità di questa frazione dimostrando che, al suo interno, si possono identificare altre due sottopopolazioni caratterizzate da una diversa fluorescenza nella lunghezza d’onda del rosso, da una diversa granulosità e da una diversa attività soppressoria. Nella seconda parte del lavoro ci siamo concentrati sulla valutazione degli effetti della chemioterapia sull’accumulo e sulla funzionalità delle MDSC, una delle principali popolazioni cellulari coinvolte nell’immunosoppressione associata ai tumori e responsabili dell’inefficacia delle terapie immunoterapiche. I dati da noi ottenuti dimostrano che, come osservato nel modello murino, l’aggiunta del 5-fluorouracile a basse dosi è in grado di indurre l’eliminazione dell’attività soppressoria delle BM-MDSC nei confronti dei linfociti T. Queste osservazioni permettono di suggerire il possibile utilizzo di alcuni chemioterapici come adiuvanti nei trattamenti immunoterapici, in quanto in grado di eliminare una delle popolazioni coinvolte nell’immunosoppressione associata ai tumori.
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Schlecker, Eva [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "The role of tumor-infiltrating MDSC subsets in tumor progression / Eva Schlecker ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2011. http://d-nb.info/1179229649/34.

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Wang, Ninghua. "Evidence for the Intermediate Phase in Bulk (K2O)x(GeO2)1-x glasses and its consequences on Electrical and Thermal Properties." University of Cincinnati / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1187020710.

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Weber, Rebekka Renate [Verfasser], and Viktor [Akademischer Betreuer] Umansky. "Regulation of CCR5 expression and immunosuppressive phenotype of MDSC in melanoma / Rebekka Renate Weber ; Betreuer: Viktor Umansky." Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1203716168/34.

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Books on the topic "MDSC"

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Massachusetts. Metropolitan District Commission. Division of Parks and Recreation. MDC bikepaths. Boston: MDC, Division of Parks and Recreation, 1986.

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Byrne, Dorena Orlagh. Data warehousing within MDS Harris. [s.l: The author], 1999.

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Resti, Benedetto Marino Di. Libro dei conti (MDXC-MDCV). Sofii︠a︡: Glavno upravlenie na arkhivite pri Ministerskii︠a︡ suvet, 2004.

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Resti, Benedetto Marino Di. Libro dei conti (MDXC-MDCV). Sofii︠a︡: Glavno upravlenie na arkhivite pri Ministerskii︠a︡ suvet, 2004.

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Hopp, Julia. The MDS troubleshooter. 2nd ed. Marblehead, MA: Opus Communications, 2002.

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Hopp, Julia. The MDS troubleshooter. 3rd ed. Marblehead, MA: HCPro, 2006.

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I, Cofer Jennifer, ed. The MDS troubleshooter. Marblehead, MA: Opus Communications, 2000.

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The MDC Shay handbook. Arlington, Wash: Oso Pub. Co., 1997.

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The MDS coordinator's field guide. Marblehead, MA: HCPro, 2007.

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Martin, Dalton &. Spettel CPA Review Course LLC. MDS CPA review: Business law. [Columbus]: Martin, Dalton & Spettel CPA Review Course, LLC, 2000.

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Book chapters on the topic "MDSC"

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Escors, David, and Grazyna Kochan. "Ex Vivo MDSC Differentiation Models." In Myeloid-Derived Suppressor Cells and Cancer, 49–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26821-7_4.

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Shibata, Masahiko, Kenji Gonda, and Seiichi Takenoshita. "MDSC: Myeloid-Derived Suppressor Cells." In Immunotherapy of Cancer, 323–34. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55031-0_22.

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Ehrenstein, Gottfried Wilhelm. "Dynamische Differenzkalorimetrie (DDK, DSC, MDSC)." In Thermische Analyse, 43–80. München: Carl Hanser Verlag GmbH & Co. KG, 2020. http://dx.doi.org/10.3139/9783446464247.003.

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De Meuter, P., H. Rahier, and B. Van Mele. "Recrystallisation of starch studied with MDSC." In Hot Topics in Thermal Analysis and Calorimetry, 49–68. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/1-4020-2219-0_3.

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Svider, Peter, Shu-Hsia Chen, Andrew G. Sikora, and Wen-Chin Yang. "Programming of MDSC: New Opportunities for Targeted Therapy." In The Tumor Immunoenvironment, 567–84. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6217-6_24.

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Sanchez-Pino, Maria Dulfary. "Detection of Circulating and Tissue Myeloid-Derived Suppressor Cells (MDSC) by Flow Cytometry." In Methods in Molecular Biology, 247–61. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1948-3_17.

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Bruderek, Kirsten, Ronja Schirrmann, and Sven Brandau. "Immunophenotyping of Circulating Myeloid-Derived Suppressor Cells (MDSC) in the Peripheral Blood of Cancer Patients." In Methods in Molecular Biology, 1–7. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-1060-2_1.

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Kochan, Grazyna. "Human MDSCs." In Myeloid-Derived Suppressor Cells and Cancer, 39–48. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26821-7_3.

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Brambilla, Marco, Jordi Cabot, and Manuel Wimmer. "MDSE Principles." In Model-Driven Software Engineering in Practice, 7–24. Cham: Springer International Publishing, 2012. http://dx.doi.org/10.1007/978-3-031-02546-4_2.

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Oette, Mark, Marvin J. Stone, Hendrik P. N. Scholl, Peter Charbel Issa, Monika Fleckenstein, Steffen Schmitz-Valckenberg, Frank G. Holz, et al. "MDS." In Encyclopedia of Molecular Mechanisms of Disease, 1270. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6247.

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Conference papers on the topic "MDSC"

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Balouek-Thomert, Daniel, Pedro Silva, Kevin Fauvel, Alexandru Costan, Gabriel Antoniu, and Manish Parashar. "MDSC." In UCC '21: 2021 IEEE/ACM 14th International Conference on Utility and Cloud Computing. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3492323.3495590.

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Cassino, Theresa R., Masaho Okada, Lauren Drowley, Johnny Huard, and Philip R. LeDuc. "Mechanical Stimulation Improves Muscle-Derived Stem Cell Transplantation for Cardiac Repair." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192941.

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Muscle-derived stem cells (MDSCs) have been successfully transplanted into both skeletal (1) and cardiac muscle (2) of dystrophin-deficient (mdx) mice, and show potential for improving cardiac and skeletal dysfunction in diseases like Duchenne muscular dystrophy (DMD). Our previous study explored the regeneration of dystrophin-expressing myocytes following MDSC transplantation into environments with distinct blood flow and chemical/mechanical stimulation attributes. After MDSC transplantation within left ventricular myocardium and gastrocnemius (GN) muscles of the same mdx mice, significantly more dystrophin-positive fibers were found within the myocardium than in the GN. We hypothesized that the differences in mechanical loading of the two environments influenced the transplantation and explored whether using MDSCs exposed to mechanical stimulation prior to transplantation could improve transplantation. Our study shows increased engraftment into the heart and GN muscle for cells pretreated with mechanical stretch for 24 hours. This increase was significant for transplantation into the heart. These studies have implications in a variety of applications including mechanotransduction, stem cell biology, and Duchenne muscular dystrophy.
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Huang., Chin-NIng. "Abstract 755: Antagonistic effect of M-MDSC and N-MDSC during astrocytoma progression." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-755.

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Cassino, Theresa R., Masaho Okada, Lauren M. Drowley, Joseph Feduska, Johnny Huard, and Philip R. LeDuc. "Using Mechanical Environment to Enhance Stem Cell Transplantation in Muscle Regeneration." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176545.

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Muscle-derived stem cell (MDSC) transplantation has shown potential as a therapy for cardiac and skeletal muscle dysfunction in diseases such as Duchenne muscular dystrophy (DMD). In this study we explore mechanical environment and its effects on MDSCs engraftment into cardiac and skeletal muscle in mdx mice and neoangiogenesis within the engraftment area. We first looked at transplantation of the same number of MDSCs into the heart and gastrocnemius (GN) muscle of dystrophic mice and the resulting dystrophin expression. We then explored neoangiogenesis within the engraftments through quantification of CD31 positive microvessels. This study is important to aid in determining the in vivo environmental factors leading to large graft size which may aid in determining optimum transplantation conditions for muscle repair.
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Hunnicutt, Ray, and David Garza. "Mission Data Storage Consolidation (MDSC)." In SpaceOps 2002 Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2002. http://dx.doi.org/10.2514/6.2002-t2-71.

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Cole, Kathryn, Holly Britton, Phyllis Warkentin, and James E. Talmadge. "Abstract 5714: SPADE identification of novel MDSC subsets." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5714.

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Calvert, Ryan D., James C. Fleet, Ye Chen, Alex Pothen, Bartek Rajwa, Pierrick G. Fournier, Patricia Juarez, Theresa A. Guise, Timothy L. Ratliff, and Ben D. Elzey. "Abstract 4741: Monocytic myeloid derived suppressor cells (M-MDSC) from spleen are multipotent while tumor M-MDSC have limited plasticity." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4741.

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Parker, Katherine, Suzanne Rosenberg, Pratima Sinha, Huan Yang, Kevin Tracey, and Jianhua Li. "Abstract 461: Inhibition of HMGB1 delays tumor progression, reduces MDSC-mediated immune suppression, and diminishes MDSC-macrophage cross-talk interaction." 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.am2013-461.

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Bryant, A. J., C. Fu, Y. Lu, M. Williams, M. Brantly, and E. Scott. "Endothelial Inflammatory Signaling Suppresses MDSC-Mediated Pulmonary Vascular Remodeling." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5282.

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Hashimoto, Ayumi, Vinit Kumar, Peter Ordentlich, and Dmitry I. Gabrilovich. "Abstract 5595: HDAC inhibitor Entinostat disrupts function of PMN-MDSC." 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.am2017-5595.

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Reports on the topic "MDSC"

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Story, Natasha Claire. Investigating the Thermal Behavior of Polymers by Modulated Differential Scanning Calorimetry (MDSC) – A Review. Office of Scientific and Technical Information (OSTI), June 2020. http://dx.doi.org/10.2172/1633549.

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Schembri, Philip, and Jillian Adams. LANL MDMC Member Update: Summer 2020. Office of Scientific and Technical Information (OSTI), July 2020. http://dx.doi.org/10.2172/1643904.

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Schembri, Philip. LANL Member Update for the 41st MDMC. Office of Scientific and Technical Information (OSTI), February 2023. http://dx.doi.org/10.2172/1923626.

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Bailey, Marcus, Lening Rivera, Alex Altunes, and Angela Walters. 5 years of lessons via MDSGC Payloads at Capitol. Ames (Iowa): Iowa State University. Library. Digital Press, January 2018. http://dx.doi.org/10.31274/ahac.11071.

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Rao, Shuyun. Study of Rpl22 in MDS and AML. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613241.

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El-Rayes, Khaled, and Ernest-John Ignacio. Evaluating the Benefits of Implementing Mobile Road Weather Information Sensors. Illinois Center for Transportation, February 2022. http://dx.doi.org/10.36501/0197-9191/22-004.

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State departments of transportation (DOTs) have traditionally utilized fixed road weather information sensors (RWIS) to improve road safety during inclement weather; enhance the management of labor, equipment, and materials for winter road maintenance; and reduce adverse environmental impacts from road maintenance activities. Despite the benefits of these fixed RWIS sites, their coverage and effectiveness are limited because of their stationary locations. To overcome these limitations, recent advances in mobile road weather information sensing technology and cellular communications have enabled the development of mobile RWIS that can be deployed on vehicles to expand the limited coverage of fixed RWIS networks. Combining mobile RWIS, fixed RWIS networks, automatic vehicle location, and maintenance decision support systems (MDSS) provide DOTs with accurate georeferenced road and weather information that can be used by DOTs to optimize winter road maintenance operations and deicer applications. This report presents the findings of a research project funded by the Illinois Department of Transportation to investigate the effectiveness of mobile RWIS and MDSS in improving winter maintenance operations. This project had the following three objectives. First, conduct a literature review to gather and analyze current practices and latest research studies on mobile RWIS and their use for collecting real-time winter roadway conditions to optimize winter maintenance operations. Second, perform interviews with other state DOTs to gather and analyze their experiences and best management practices for the deployment and use of mobile RWIS and MDSS. Third, develop recommendations for a pilot study to evaluate the deployment and performance of mobile RWIS and MDSS in order to determine their effectiveness, implementation requirements, software/technology needs, operational challenges, and life-cycle costs.
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Precoda, K., and T. Meng. Long-term Stability of Listening Strategies Determined by MDS. Fort Belvoir, VA: Defense Technical Information Center, May 1998. http://dx.doi.org/10.21236/ada357785.

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Shelley, John, Christopher Haring, and Nathan Chrisman. Evaluation of cedar tree revetments for bank stabilization at the Locust Creek Conservation Area, Missouri : quantifying bank erosion volumes from preproject to postfailure. Engineer Research and Development Center (U.S.), December 2022. http://dx.doi.org/10.21079/11681/46144.

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The US Army Corps of Engineers Regional Sediment Management (RSM) program funded research to assess the longevity and effectiveness of cedar tree revetments for sediment reduction. Between 1988 and 1997, the Missouri Department of Conservation (MDC) constructed multiple cedar tree revetments, plantings, and a grade-control structure at an experimental stream management area on Locust Creek within the Locust Creek Conservation Area (LCCA). For the first few years, MDC also replaced missing trees as needed. MDC monitored these sites with photographs and cross sections until 2004. This study evaluated bank stability on Locust Creek from 1970 to 2019 using aerial imagery, lidar, ground surveys, and a December 2019 site visit to estimate the areal change in streambanks and the volume of sediment eroded over the years. Based on their dates of construction, the project compared preproject, with-project, and postfailure conditions at each site. The project included cedar tree revetments, other hardwood revetments, plantings, and a grade-control structure. This research found a 50% to 64% reduction in erosion for approximately 14 years. As of December 2019, all tree revetments had failed, and banks were bare and steep. The grade-control structure remained intact and continued to stabilize bed and banks immediately upstream.
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Verma, Amit. Meta-Analytical Online Repository of Gene Expression Profiles of MDS Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada603210.

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Guan, X., and E. C. Uberbacher. A multiple divide-and-conquer (MDC) algorithm for optimal alignments in linear space. Office of Scientific and Technical Information (OSTI), June 1994. http://dx.doi.org/10.2172/10168027.

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