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Relevant bibliographies by topics / Bone Marrow Dendritic Cells

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Academic literature on the topic 'Bone Marrow Dendritic Cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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Journal articles on the topic "Bone Marrow Dendritic Cells"

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Wang, Quanxing, Weiping Zhang, Guoshan Ding, Lifei Sun, Guoyou Chen, and Xuetao Cao. "DENDRITIC CELLS SUPPORT HEMATOPOIESIS OF BONE MARROW CELLS1." Transplantation 72, no. 5 (September 2001): 891–99. http://dx.doi.org/10.1097/00007890-200109150-00026.

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Baba, Susumu, Muneo Inaba, Hiroshi Iwai, Mitsuru Taira, Keizo Takada, Hiroko Hisha, Toshio Yamashita, and Susumu Ikehara. "Intra-bone marrow-bone marrow transplantation facilitates hemopoietic recovery including dendritic cells." Immunobiology 210, no. 1 (July 2005): 33–42. http://dx.doi.org/10.1016/j.imbio.2005.02.005.

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Leone, Patrizia, Simona Berardi, Maria Antonia Frassanito, Roberto Ria, Valli De Re, Sebastiano Cicco, Stefano Battaglia, et al. "Dendritic cells accumulate in the bone marrow of myeloma patients where they protect tumor plasma cells from CD8+ T-cell killing." Blood 126, no. 12 (September 17, 2015): 1443–51. http://dx.doi.org/10.1182/blood-2015-01-623975.

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Baru, Abdul Mannan, Jayendra Kumar Krishnaswamy, Anchana Rathinasamy, Michaela Scherr, Matthias Eder, and Georg M. N. Behrens. "Dendritic cells derived from HOXB4-immortalized hematopoietic bone marrow cells." Experimental Biology and Medicine 236, no. 11 (November 2011): 1291–97. http://dx.doi.org/10.1258/ebm.2011.011140.

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Dendritic cells (DCs) are essential for the generation and modulation of cell-mediated adaptive immunity against infections. DC-based vaccination involves transplantation of ex vivo-generated DCs loaded with antigen in vitro, but remains limited by the number of autologous or allogeneic cells. While in vitro expansion and differentiation of hematopoietic stem cells (HSCs) into DCs seems to be the most viable alternative to overcome this problem, the complexity of HSC expansion in vitro has posed significant limitations for clinical application. We immortalized lineage-depleted murine hematopoietic bone marrow (lin−BM) cells with HOXB4, and differentiated them into CD11c+MHCII+ DCs. These cells showed the typical DC phenotype and upregulated surface expression of co-stimulatory molecules on stimulation with various toll-like receptor ligands. These DCs efficiently presented exogenous antigen to T-cells via major histocompatibility complex (MHC) I and II and viral antigen on infection. Finally, they showed migratory capacity and were able to generate antigen-specific primed T-cells in vivo. In summary, we provide evidence that HOXB4-transduced lin−BM cells can serve as a viable means of generating fully functional DCs for scientific and therapeutic applications.

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Bowers, W. E., and M. R. Berkowitz. "Differentiation of dendritic cells in cultures of rat bone marrow cells." Journal of Experimental Medicine 163, no. 4 (April 1, 1986): 872–83. http://dx.doi.org/10.1084/jem.163.4.872.

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Although dendritic cells (DC) originate from bone marrow, they were not observed in fresh preparations of bone marrow cells (BMC). Likewise, accessory activity was barely measurable in a sensitive assay for this potent function of DC. However, both DC and accessory activity developed when BMC were cultured for 5 d. Based on fractionation before culture, nearly all of the accessory activity could be attributed to only 5% of the total BMC recovered in a low-density (LD) fraction. The LD-DC precursors differed from mature DC in a number of important respects. Removal of Ia+ cells from the LD fraction by panning did not decrease the production of DC when the nonadherent cells were cultured. Thus, the cell from which the DC is derived does not express or minimally expresses Ia antigens, in contrast to the strongly Ia+ DC that is produced in bone marrow cultures. Irradiation of LD cells before culture prevented the development of DC. When irradiation was delayed by daily intervals, progressive increases in the number of DC resulted, up to the fifth day. These findings, together with preliminary autoradiographic data, indicate that cell division has occurred, in contrast to the DC, which does not divide. We conclude that bone marrow-derived DC arise in culture from the division of LD, Ia- precursors.

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Zuniga, Elina I., Dorian B. McGavern, Jose L. Pruneda-Paz, Chao Teng, and Michael B. A. Oldstone. "Bone marrow plasmacytoid dendritic cells can differentiate into myeloid dendritic cells upon virus infection." Nature Immunology 5, no. 12 (November 7, 2004): 1227–34. http://dx.doi.org/10.1038/ni1136.

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O’Keeffe, Meredith, Ben Fancke, Mark Suter, Georg Ramm, Joan Clark, Li Wu, and Hubertus Hochrein. "Nonplasmacytoid, High IFN-α–Producing, Bone Marrow Dendritic Cells." Journal of Immunology 188, no. 8 (March 14, 2012): 3774–83. http://dx.doi.org/10.4049/jimmunol.1101365.

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Yu, Shaohua, Cunren Liu, Kaihong Su, Jianhua Wang, Yuelong Liu, Liming Zhang, Chuanyu Li, et al. "Tumor Exosomes Inhibit Differentiation of Bone Marrow Dendritic Cells." Journal of Immunology 178, no. 11 (May 18, 2007): 6867–75. http://dx.doi.org/10.4049/jimmunol.178.11.6867.

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Iijima, N., M. M. Linehan, S. Saeland, and A. Iwasaki. "Vaginal epithelial dendritic cells renew from bone marrow precursors." Proceedings of the National Academy of Sciences 104, no. 48 (November 15, 2007): 19061–66. http://dx.doi.org/10.1073/pnas.0707179104.

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knight, Stella C. "Bone-marrow-derived dendritic cells and pathogenesis of AIDS." AIDS 10, no. 8 (July 1996): 807–18. http://dx.doi.org/10.1097/00002030-199607000-00003.

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Dissertations / Theses on the topic "Bone Marrow Dendritic Cells"

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Powell, Timothy Jack. "Characterisation of rat bone marrow derived dendritic cells." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298613.

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Raveney, Ben J. E. "Interactions between CD8+ T cells and bone marrow-derived dendritic cells." Thesis, University of Bristol, 2006. http://hdl.handle.net/1983/dbbc656f-a103-4787-aeb9-f203c3f0082b.

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Li, Yanli. "Characterisation of PRRSV1 infection in bone marrow-derived dendritic cells." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458631.

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Esta tesis tiene como objeto caracterizar la adhesión, la replicación y la inducción de apoptosis en células dendríticas inmaduras (i) y maduras (m) derivadas de médula ósea (BMDC) enfrentadas al virus del PRRS (VPRRS). Se utilizaron tres aislados de PRRSV1 (3249, 3262 y 3267) cuya cinética de replicación se determinó inicialmente en macrófagos alveolares porcinos (PAM). El título obtenido en iBMDC fue significantemente mayor que en mBMDC (12 y 24hpi). Para los aislados 3249 y 3262, la replicación alcanzó el pico antes en las iBMDC (24h) que en las mBMDC (48h). Además, la eficacia de replicación dependía de la cepa usada siendo la cepa 3262 la que siempre tuvo menor replicación e infectó a una menor proporción de células. El estudio de adhesión y replicación con relación a la expresión de tres receptores: PoSn, CD163 y sulfato de heparán, se estudió mediante microscopía confocal de tres colores (PoSn, CD163 and PRRSV), y reveló que en iBMDC existía adhesión en las 4 subpoblaciones definidas por PoSn y CD163, incluso después del bloqueo del sulfato de heparán. Estos resultados sugerían la posibilidad de que existieran otros receptores víricos. Seguidamente, se realizó un estudio de microscopía confocal con marcaje de CD163/PRRSV o PoSn/PRRSV, observándose replicación en células aparentemente PoSn- y CD163-. A continuación se estudió la expresión de CD163 en las iBMDC infectadas por la cepa 3267 mediante citometría. Es este caso, el 8.4±0.5% de células aparentemente CD163- se marcaron como infectadas. Tras esto, se realizó una separación por citometría de flujo en función de la expresión de CD163 (CD163-, CD163lo and CD163hi). La primera separación se centró en aquellas CD163- cuya clasificación estaba "más allá de la duda". La segunda, se enfocó en el grupo de células CD163- junto con CD163lo. Como controles se emplearon iBMDC sin separar. No se observó infección en las células CD163- “más allá de la duda”. Cuando las CD163- se clasificaron junto con células CD163lo, la población CD163- infectada fue de 0,6 ± 0,07% a las 40 hpi aumentando a 1,6% ± 0,08% a las 60 hpi, siendo la proporción de células infectadas mayor que el número inicial de células CD163+. Este hecho podría ser debido a la generación de nuevas células CD163lo que se infectarían tan pronto como expresaran esta molécula, o alternativamente, el medio creado por la infección de células CD163+ indujo la aparición de la población CD163- susceptible. El estudio de inducción de la apoptosis, en PAM se observó un marcaje positivo para la caspasa-3 activada tanto en células infectadas como no infectadas para los tres aislamientos (microscopía confocal). Por el contrario, en BMDC el marcaje se localizó principalmente en células no infectadas. Este hallazgo sugiere la diferente activación de las vías intrínseca y extrínseca para PAMs y BMDC. Además, la señal de caspasa-3 en BMDC alcanzó un máximo a las 48 hpi, más tarde que en PAM (24 hpi). Este desarrollo más lento de la apoptosis podría permitir más ciclos de replicación vírica, resultando en mayores rendimientos víricos en BMDC. Un examen posterior para apoptosis/necrosis de cultivos de BMDC mostró que los aislados 3249 y 3267 indujeron apoptosis y necrosis, mientras que 3262 sólo produjo cambios menores. La neutralización de la IL-10 inducida por el 3262 dio lugar a la aparición de células apoptóticas, pero este efecto no ocurrió con 2988 que inducía también la producción de IL-10. Por lo tanto, todavía no está claro el papel de IL-10 juega en la apoptosis inducida por PRRSV. Los resultados de esta tesis pueden ser útiles para comprender el papel de DC en la patogénesis de PRRSV.
The present thesis aims to characterize the attachment, replication and the induction of apoptosis during PRRSV infection in immature (i) and mature (m) bone marrow-derived dendritic cells (BMDC). Three PRRSV1 isolates (3249, 3262 and 3267) were used. The kinetics of replication were assessed by titrating cell culture supernatants in macrophages. The viral yield in iBMDC at 12 and 24 hpi was significantly higher than in mBMDC, and the replication of two isolates (3249 and 3262) peaked earlier in iBMDC (24 hpi) compared to mBMDC (48hpi). These results indicated that iBMDC were more efficient than mBMDC in supporting viral replication. This feature was not related to the proportion of CD163+ cells nor the levels of IFN-α in the cultures. In addition, the replication efficiency was strain-dependent. Isolate 3262 showed the lowest titres in both cell types at all times, consistently with the lowest proportions of 3262-infected cells in flow cytometry. The attachment and replication was further studied in association with the expression of three receptors, PoSn, CD163 and heparan sulphate. A three-colour confocal microscopy staining (PoSn, CD163 and PRRSV) on iBMDC showed that attachment occurred on the four subsets defined by PoSn and CD163. Removal of heparan sulphate from the cell surface did not fully avoid the attachment. These results indicated that attachment of PRRSV1 on BMDC might occur beyond the intervention of heparan sulphate, PoSn and CD163 and point towards the existence of other potential receptors. Next, a two-colour confocal microscopy labelling CD163/PRRSV or PoSn/PRRSV was performed. Replication was observed in cells that were apparently PoSn- and CD163-. As CD163 is the only recognized essential receptor for PRRSV, its expression together with the infection by isolate 3267 on iBMDC was further examined by flow cytometry. In that case, 8.4 ± 0.5% of apparently CD163- cells were labelled as infected. To further clarify this, a sorting experiment based on CD163 expression (CD163-, CD163lo and CD163hi) was done. The first sorting focused on “beyond doubt” CD163- cells. The second sorting grouped CD163- cells together with CD163lo. Unsorted iBMDC were used as controls. The “beyond doubt” CD163- cells were not infected by 40 hpi. When CD163- were sorted together with CD163lo, the proportion of infected CD163- cells was 0.6 ± 0.07% at 40 hpi and 1.6% ± 0.08% at 60 hpi. The proportion of infected cells at 60 hpi was higher than the initial number of CD163+ cells. These results can be explained by the generation of new CD163lo that were probably infected when expressing levels of this molecule below the sensitivity of the cytometer. Alternatively, the milieu created by CD163+ infected cells resulted in CD163- susceptible cells expressing yet unknown receptors for the virus. Regarding the induction of apoptosis, in PAM cleaved caspase-3 labelling was observed in both infected and bystander cells for all three isolates (confocal microscopy), while in BMDC bystanders were mainly labelled. This is indicative of different apoptosis triggering pathways for PAM and BMDC. Moreover, at m.o.i. 0.1, the caspase-3 signal in BMDC peaked later (48 hpi) than in PAM (24 hpi), which might allow more cycles of viral replication and result in higher viral yields in BMDC. Further examination of inoculated BMDC cultures for apoptosis/necrosis showed significant differences between isolates. Thus, 3249 and 3267 isolates apparently induced apoptosis/necrosis of BMDC but 3262 did not. Neutralization of IL-10 released by BMDC and induced by 3262 infection resulted in the occurrence of apoptotic cells, but this did not happen with a second IL-10-inducing isolate (2988). The above-mentioned results will be useful to understand the role of DC in PRRSV pathogenesis.

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Liu, Limin 1954. "Expression of follicular dendritic cell determinants by mouse bone marrow stromal cells." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27544.

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Stromal reticular cells in mouse bone marrow and follicular dendritic cells (FDC) in peripheral lymphoid tissues both interact with B lymphocytes and influence their development at various stages of the B cell lineage. The possibility that BM reticular cells and FDCs may share common surface properties has been examined in mouse bone marrow by in vivo administration of $ sp{125}$I-labelled purified monoclonal antibodies (mAb) raised against mouse FDC, detecting mAb-binding by light microscope (LM) and electron microscope (EM) radioautography. Young mice were injected intravenously with $ sp{125}$I-mAb FDC-M1, FDC-M2, FDC-M3 and then perfused to remove unbound antibody. Quantitative analyses of radioautographic LM sections of femoral bone marrow revealed discrete FDC-labelling throughout bone marrow sections, especially in outer areas near the surrounding bone and intermediate areas, forming both linear arrangements and irregular patches. Electron microscopy revealed labelling aligned over delicate processes of certain reticular cells intimately associated with lympho hemopoietic cells, as well as localized regions of sinusoidal endothelium, particularly in central areas and at sites of contact with hemopoietic cells. The results demonstrate that a subset of stromal reticular cells in mouse BM express FDC-associated surface determinants, suggesting possible common lineage or functional properties.

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Liu, Limin. "Expression of follicular dendritic cell determinants by mouse bone marrow stromal cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ37142.pdf.

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Colledge, Lisa H. "Investigation of antigen presentation by murine bone marrow-derived dendritic cells." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312678.

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Maroof, Asher. "The effects of IL-4 on murine bone marrow derived dendritic cells." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398141.

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Chan, Shing, and 陳誠. "Generation and functional characterization of dendritic cells from bone marrow of patients with leukaemia diseases and various haemato-oncological conditions." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970394.

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Chan, Shing. "Generation and functional characterization of dendritic cells from bone marrow of patients with leukaemia diseases and various haemato-oncological conditions." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25176511.

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Kohara, Hiroshi. "Development of plasmacytoid dendritic cells in bone marrow stromal cell niches requires CXCL12-CXCR4 chemokine signaling." Kyoto University, 2008. http://hdl.handle.net/2433/135825.

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Books on the topic "Bone Marrow Dendritic Cells"

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Thomas, Gethin Penar. Load responsiveness of bone marrow stromal cells. Birmingham: University of Birmingham, 1994.

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Pathology of bone marrow and blood cells. 2nd ed. Baltimore, Md: Lippincott William & Wilkins, 2009.

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Pathology of bone marrow. 2nd ed. Baltimore: Williams & Wilkins, 1998.

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Pathology of bone marrow. New York, N.Y: Igaku-Shoin, 1992.

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Cherry, Daniel A. Bone marrow: A practical manual. Austin, Tex: Landes Bioscience, 2011.

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Miszta, Helena. Fizjologiczna rola komórek mikrośrodowiska szpiku kostnego--stymulatory i inhibitory ich wzrostu. Kraków: Nakł. Uniwersytetu Jagiellońskiego, 1992.

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Gulati, Subhash C. Purging in bone marrow transplantation. Austin: R.G. Landes Co., 1993.

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Diggs, L. W. The morphology of human blood cells. 6th ed. Abbott Park, Ill: Abbott Laboratories, 2003.

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Chu, Jennifer. Enhanced engraftment of genetically modified bone marrow stromal cells. Ottawa: National Library of Canada, 2001.

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Oboznai͡a, Ė. I. T͡Sitokhimii͡a kostnogo mozga pri kriokonservirovanii: Atlas. Kiev: Nauk. dumka, 1989.

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Book chapters on the topic "Bone Marrow Dendritic Cells"

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Roney, Kelly. "Bone Marrow-Derived Dendritic Cells." In Mouse Models of Innate Immunity, 71–76. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-481-4_9.

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Roney, Kelly. "Bone Marrow-Derived Dendritic Cells." In Mouse Models of Innate Immunity, 57–62. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9167-9_4.

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Penchansky, Lila. "Macrophage- and Dendritic-Cell-Related Disorders Including the Lysosomal Storage Disorders." In Pediatric Bone Marrow, 47–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18799-5_3.

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Bowers, William E., and Mary R. Berkowitz. "Development of Dendritic Cells from Rat Bone Marrow." In Microenvironments in the Lymphoid System, 377–81. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2463-8_45.

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Shimamura, Hiromune, Fuyuhiko Motoi, Jun-Ichiro Yamauchi, Kazuhiko Shibuya, Makoto Sunamura, Kazunori Takeda, and Seiki Matsuno. "Cytotoxic Effect of Bone Marrow-Derived Dendritic Cells." In Trends in Gastroenterology and Hepatology, 167–70. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-67895-3_30.

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Indrová, Marie, Luis Mendoza, Milan Reiniš, Vladimír Vonka, Michal Šmahel, Šárka Némecková, Táňa Jandlová, and Jan Bubeník. "Bone marrow dendritic cell-based anticancer vaccines." In Advances in Experimental Medicine and Biology, 355–58. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0685-0_50.

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Zhao, Chen, and Zenggang Pan. "Histiocytic/Dendritic Cell Neoplasms: Primary and Transdifferentiated." In Practical Lymph Node and Bone Marrow Pathology, 345–54. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-32189-5_17.

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Hochrein, Hubertus, Frank Jährling, H. Georg Kreysch, and Arne Sutter. "Immunophenotypical and Functional Characterization of Bone Marrow Derived Dendritic Cells." In Advances in Experimental Medicine and Biology, 61–63. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_12.

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Onai, Nobuyuki, and Toshiaki Ohteki. "Isolation of Dendritic Cell Progenitor and Bone Marrow Progenitor Cells from Mouse." In Methods in Molecular Biology, 53–59. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3606-9_4.

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Chen-Woan, Melissa, Conor P. Delaney, Veronique Fournier, Yoshitaka Wakizaka, Noriko Murase, Angus W. Thomson, John J. Fung, Thomas E. Starzl, and Anthony J. Demetris. "A Simplified Method for Growing Dendritic Cells from Rat Bone Marrow." In Advances in Experimental Medicine and Biology, 53–55. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_10.

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Conference papers on the topic "Bone Marrow Dendritic Cells"

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Xu, Shuyun, Juihung Yen, Doina Ganea, and Kwang Chul Kim. "The Role Of Muc1 Mucin In Bone Marrow-Derived Dendritic Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2843.

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Sun, Guolong, Xin Fu, Kaizhong Wang, Hui Zhao, and Dengli Wang. "Culture and identification of dendritic cells from mouse bone marrow in vitro." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027886.

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Porto, Barbara N., Ana Paula D. Souza, James Crowe, Fernando P. Polack, Renato T. Stein, and Cristina Bonorino. "Modulation Of Murine Bone Marrow-Derived Dendritic Cells By H1N1 Virus Hemagglutinins." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5712.

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Gray, Kelsey, Laura A. Warg, Judy L. Oakes, Ivana V. Yang, Ross M. Kedl, E. R. Sutherland, Brian P. O'Connor, and David A. Schwartz. "Dietary Vitamin D Modulates MHC Class LI Expression And Function In Bone Marrow Derived Dendritic Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2839.

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So, Eui Young, and Toru Ouchi. "Abstract 3088: Essential roles of ATM in GM-CSF-induced bone marrow differentiation to dendritic cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3088.

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Page, Kristen, Ping Zhou, and John Ledford. "Severe Sepsis Reprograms Bone Marrow Derived Dendritic Cells Resulting In Decreased Sensitivity To Secondary Exposure In A Murine Model." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2214.

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Chen, Zhihong, Kan Xu, Nan Wu, Zhihui Min, and Zhilong Jiang. "Bone marrow derived dendritic cell (BMDC) adoptive transfer alleviate OVA-induced allergic airway inflammation in asthmatic mice." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2045.

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Chen, Z., K. Xu, N. Wu, Z. Min, and Z. Jiang. "Bone Marrow Derived Dendritic Cell (BMDC) Adoptive Transfer Alleviate Ova-Induced Allergic Airway Inflammation in Asthma Mice." 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.a2900.

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Liu, Ping, Xiaomin Ren, and Lisa X. Xu. "Alternate Cooling and Heating Thermal Physical Treatment: An Effective Strategy Against MDSCs in 4T1 Mouse Mammary Carcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80229.

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An alternate thermal physical treatment was developed to destroy tumor tissue using liquid nitrogen cooling and RF heating treatment in our pervious study. Our pervious reports had shown that anti-tumor immunity was induced by the alternate treatment. Myeloid derived suppressor cells (MDSCs) are a subset of heterogeneous, bone marrow derived hematopoietic cells that accumulate in the spleen, bone marrow, blood and tumor sites of tumor-bearing mice and cancer patients. MDSCs are one of the key suppressor cells that regulate anti-tumor immune responses in tumor-bearing hosts. MDSCs have been shown to inhibit the function of various types of cells mediating anti-tumor immunity, such as T cells, B cells, NK cells and dendritic cells. MDSCs are recruited specifically to the tumors and contribute indirectly to angiogenesis, growth and metastasis. MDSCs also exert resistance to cancer therapies, such as anti-VEGF strategies and cancer immunotherapy. Given the role of MDSCs in tumor invasion and metastasis and anti-tumor immune responses, therapeutics targeting MDSCs might offer a new strategy for cancer treatment. In this study, the therapeutic effect and MDSCs changes after the alternate cooling and heating treatment was studied using the 4T1 murine mammary carcinoma, a common animal model of human metastatic breast cancer. Due to its highly invasive and poorly immunogenic characters, the 4T1 tumor could cause death even after the primary tumor was surgically removed. The treatment was carried out when micro-metastases were well established. Comparisons were made with the results from the surgery and hyperthermia groups, respectively. The results showed that MDSCs in blood increased rapidly with time after tumor inoculation, and in 66 days, all the mice died in the control group. The statistical results indicated a significant increase in circulating MDSC numbers at different tumor growth stages. In the surgical resection group, MDSCs in blood did not decrease, but increased rapidly to a level much higher that of the control group in 39 day after tumor inoculation. In the hyperthermia group, MDSCs in blood increased rapidly with time after tumor inoculation, and in 39 day, MDSCs was up to 3 times higher than that of the control group. Mice died in 45 day after initial tumor inoculation. But in the alternate treatment group, the number of MDSCs decreased rapidly and recovered to the normal healthy level in 11 days after the treatment. No metastatic tumor could be observed in these mice, and they were in good physiological conditions as observed in the following 3 month. In conclusion, the alternate treatment was found extremely effective against MDSCs in the very aggressive and highly metastatic mouse mammary carcinoma. The good prognosis was expected in relation to the significant decrease in MDSCs and thus the relief of the immune suppression, induced by the alternate cooling and heating treatment. It could be further developed as a novel therapeutic method against metastatic tumor. On the other hand, combining the alternate treatment with other strategies, such as anti-VEGF and cancer immunotherapy, the best therapeutic effect would be achieved through synergy.

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Sayo, Kanae, Shigehisa Aoki, and Nobuhiko Kojima. "A method to reorganize the bone marrow-like tissue with suspension of bone marrow cells." In 2015 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2015. http://dx.doi.org/10.1109/mhs.2015.7438268.

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Reports on the topic "Bone Marrow Dendritic Cells"

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Dooner, Mark, Jason M. Aliotta, Jeffrey Pimental, Gerri J. Dooner, Mehrdad Abedi, Gerald Colvin, Qin Liu, Heinz-Ulli Weier, Mark S. Dooner, and Peter J. Quesenberry. Cell Cycle Related Differentiation of Bone Marrow Cells into Lung Cells. Office of Scientific and Technical Information (OSTI), December 2007. http://dx.doi.org/10.2172/936517.

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Park, Serk I. Activation of Myeloid-Derived Suppressor Cells in Bone Marrow. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada600504.

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Wieder, Robert. Overcoming Bone Marrow Stroma-Mediated Chemoresistance in Metastatic Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada429152.

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Cox, Jr, and Charles S. Treatment of Adult Severe Traumatic Brain Injury Using Autologous Bone Marrow Mononuclear Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada609600.

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Patrick Frost, PhD, Patrick Frost, PhD. Targeting the Hypoxic Response in Multiple Myeloma Cells Engrafted in the Bone Marrow. Experiment, December 2015. http://dx.doi.org/10.18258/6331.

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Cox, Charles. Treatment of Adult Severe Traumatic Brain Injury Using Autologous Bone Marrow Mononuclear Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada570264.

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Cox, Jr, and Charles S. Treatment of Adult Severe Traumatic Brain Injury Using Autologous Bone Marrow Mononuclear Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada584217.

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Cox, Jr, and Charles S. Treatment of Adult Severe Traumatic Brain Injury Using Autologous Bone Marrow Mononuclear Cells. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada619276.

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Gupta, Piyush, and Robert A. Weinberg. Contribution of Bone Marrow-Derived Cells to the Tumor Stroma in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada417609.

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Gupta, Piyush, and Robert A. Weinberg. Contribution of Bone Marrow-Derived Cells to the Tumor Stroma in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada428526.

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