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Journal articles on the topic 'Bone Marrow Dendritic Cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

ISOTANI, Mayu, Kensuke KATSUMA, Kyoichi TAMURA, Misato YAMADA, Hiroko YAGIHARA, Daigo AZAKAMI, Kenichiro ONO, Tsukimi WASHIZU, and Makoto BONKOBARA. "Efficient Generation of Canine Bone Marrow-Derived Dendritic Cells." Journal of Veterinary Medical Science 68, no. 8 (2006): 809–14. http://dx.doi.org/10.1292/jvms.68.809.

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12

Zhang, Jingzhu, Daniel C. Link, Teerawit Supakorndej, and Mahil Rao. "Myeloid Dendritic Cells Contribute to Hematopoietic Homeostasis." Blood 128, no. 22 (December 2, 2016): 30. http://dx.doi.org/10.1182/blood.v128.22.30.30.

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Abstract Dendritic cells (DCs) are antigen-presenting cells that are distributed throughout the body, and their main function is thought to be immune-surveillance. There is considerable phenotypic and functional heterogeneity of dendritic cells that tracks, in part, with their tissue localization. Myeloid dendritic cells (mDC), also known as conventional dendritic cells, are DCs with a myeloid origin. A previous study showed that perivascular mDCs in the bone marrow provide signals that regulate the survival of mature B cells (Sapoznikov et al., Nat Immunol, 2008). Using Cx3cr1gfp/+mice, we show that mDCs, defined as CX3CR1-GFP-bright, MHCII-bright cells, represent 0.2 ± 0.08% of bone marrow cells. They are localized to both venous sinusoids and arterioles in the bone marrow, placing them in the perivascular stem niche, along with CXCL12-abundant reticular (CAR) cells and Nestin-GFP+ cells. To assess the contribution of mDCs to the regulation of hematopoiesis, we used two independent mouse models to ablate mDCs: CD11cDTR and Zbtb46DTR mice. We previously reported that ablation of mDCs induces modest hematopoietic stem/progenitor (HSPC) mobilization. We show that mDC ablation also suppresses osteoblast function, with expression of osteocalcin mRNA (a marker of mature osteoblasts) decreasing 3.5-fold after mDC ablation (from 18.7 ± 9.9 to 5.3 ± 3.0; P < 0.05). To our surprise, mDC ablation (in both models) was associated with a significant loss of bone marrow macrophages. Prior studies have shown that macrophage ablation results in a loss of mature osteoblasts and modest HPSC mobilization. Thus, it is not clear whether mDCs have an independent effect on HSPC trafficking and osteoblast function. To address this issue, we first asked whether the macrophage loss after mDC ablation was mediated in a non-cell autonomous fashion. Mixed bone marrow chimeras were established containing both Zbtb46DTR and wild-type hematopoietic cells. Upon treatment with diphtheria toxin, we observed depletion of Zbtb46DTR but not wild-type mDCs (as expected). In contrast, a similar decrease in both Zbtb46DTR and wild-type macrophages was observed. These data show that the decrease in macrophages is an indirect consequence of mDC ablation and suggest that mDCs generate signals that contribute to macrophage retention and/or survival in the bone marrow. To further address the role of macrophages in this phenotype, we generated mice expressing Zbtb46-DTR alone, CD169-DTR alone (previously shown to ablate macrophages), or mice carrying both Zbtb46-DTR and CD169-DTR. As reported previously, ablation of macrophages induces a modest mobilization of Kit+ Sca1+ lineage- (KSL) cells to the spleen (7.1 ± 3.2 x104 versus 3.0 ± 1.2 x104 for PBS treated mice; P =0.06). Ablation of mDCs also induces modest mobilization (9.1 ± 2.5 x104 versus 5.8 ± 3.5 x104 for PBS treated mice; P < 0.05). Preliminary analysis of double mutant mice (n = 4) suggest an additive effect of combined mDC and macrophage ablation on HSPC mobilization with 25.9 ± 18.4 x104 KSL cells per spleen (P < 0.05 compared with macrophage alone ablation). Likewise, preliminary analysis suggests that the magnitude of osteoblast suppression (as measured by osteocalcin expression) is greater in double mutant mice. Collectively, these data suggest that bone marrow mDCs, in addition to a possible role in immune surveillance, contribute to blood homeostasis through multiple mechanisms. Specifically, mDCs appear to generate signals that are required for macrophage retention and/or survival in the bone marrow. mDCs also regulate HSPC trafficking and osteoblast function through a macrophage independent mechanism. Studies are underway to identify signals generated by mDCs that mediate these biological responses. Disclosures No relevant conflicts of interest to declare.

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13

Supakorndej, Teerawit, Mahil Rao, and Daniel C. Link. "Myeloid Dendritic Cells Regulate HSPC Trafficking In The Bone Marrow." Blood 122, no. 21 (November 15, 2013): 584. http://dx.doi.org/10.1182/blood.v122.21.584.584.

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Abstract Granulocyte-colony stimulating factor (G-CSF) is the prototypic agent used to mobilize hematopoietic stem and progenitor cells (HSPCs) into the blood where they can then be harvested for stem cell transplantation. G-CSF acts in a non-cell-intrinsic fashion to induce HSPC mobilization. We recently showed that G-CSF signaling in a CD68+ monocyte/macrophage lineage cell within the bone marrow initiates the HSPC mobilization cascade (Christopher et al., 2011). CD68 marks a heterogeneous cell population that includes monocytes, macrophages, myeloid dendritic cells, and osteoclasts. Within the bone marrow, myeloid dendritic cells (MDCs) are found perivascularly and in close association with CXCL12-abundant reticular (CAR) cells, suggesting a role for MDCs in maintaining HSPC niche function. We previously reported that G-CSF treatment (250 µg/kg per day for 5 days) suppresses macrophage (11.8 ± 3.6-fold) and myeloid dendritic cell (MDCs; 5.5 ± 1.2-fold) numbers in the bone marrow (Supakorndej et al., ASH abstract #2319, 2012). Moreover, we showed that CD11c-DTR mediated MDC ablation results in a modest mobilization of HSPCs. However, CD11c-DTR ablates bone marrow macrophages, as well as MDCs, so a definitive role for MDCs in G-CSF-induced HSPC mobilization could not be established. To address this concern, we used transgenic mice expressing the diphtheria toxin receptor under the control of the Zbtb46 promoter (Zbtb46-DTR). A prior study demonstrated that Zbtb46 is expressed specifically in MDCs but not macrophages nor other immune cell lineages in peripheral lymphoid tissues (Satpathy et al., 2012). Using Zbtb46gfp/+ mice, we likewise found that Zbtb46 is expressed in bone marrow MDCs but not bone marrow macrophages. Finally, a recent study showed that Zbtb46-DTR specifically ablates MDCs (Meredith et al., 2012). To avoid systemic toxicity, we transplanted Zbtb46-DTR bone marrow into congenic wild-type recipients. The resulting bone marrow chimeras were treated with diphtheria toxin (DT; 400 ng per day for 6 days), which resulted in an 82% reduction of MDCs in the bone marrow. MDC ablation resulted in significant mobilization of colony-forming cells (figure 1A) and c-Kit+lineage-Sca-1+ (KLS) cells (figure 1B) into the blood and spleen. Moreover, MDC ablation enhanced mobilization of these cells by G-CSF (figures 1C and 1D). Together with the CD11c-DTR mice, the Zbtb46-DTR studies provide strong evidence that MDCs contribute to G-CSF-induced HSPC mobilization.Figure 1HSPC mobilization in Zbtb46-DTR mice. Zbtb46-DTR bone marrow chimeras were treated with diphtheria toxin (DT) alone, G-CSF alone, or DT plus G-CSF. The number of CFU-C (A & C) or KLS cells (B & D) in the blood and spleen are shown. Data represent the mean ± SEM of 5 mice from one experiment. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.Figure 1. HSPC mobilization in Zbtb46-DTR mice. Zbtb46-DTR bone marrow chimeras were treated with diphtheria toxin (DT) alone, G-CSF alone, or DT plus G-CSF. The number of CFU-C (A & C) or KLS cells (B & D) in the blood and spleen are shown. Data represent the mean ± SEM of 5 mice from one experiment. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. We previously showed that G-CSF mobilizes HSPCs, at least in part, by decreasing CXCL12 expression in bone marrow stromal cells. We found that MDC ablation (using CD11c-DTR mice) also suppresses CXCL12 expression in the bone marrow (35.2 ± 18.1% reduction). We recently reported that CXCL12 expression from perivascular stromal cells (including mesenchymal progenitors, CAR cells, and endothelial cells) is required for HSC maintenance (Greenbaum et al., 2013). Here, we show that G-CSF suppresses CXCL12 mRNA expression in both CAR cells and endothelial cells. Surprisingly, preliminary data suggest that MDC ablation does not affect CAR cell number nor CXCL12 expression in these cells. Studies are in progress to assess the effect of MDC ablation on endothelial CXCL12 expression. Collectively, these data suggest that MDC-derived signals contribute to HSPC maintenance by modulating stromal cells that comprise the perivascular niche. Disclosures: No relevant conflicts of interest to declare.

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14

Inaba, K., M. Inaba, N. Romani, H. Aya, M. Deguchi, S. Ikehara, S. Muramatsu, and R. M. Steinman. "Generation of large numbers of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor." Journal of Experimental Medicine 176, no. 6 (December 1, 1992): 1693–702. http://dx.doi.org/10.1084/jem.176.6.1693.

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Antigen-presenting, major histocompatibility complex (MHC) class II-rich dendritic cells are known to arise from bone marrow. However, marrow lacks mature dendritic cells, and substantial numbers of proliferating less-mature cells have yet to be identified. The methodology for inducing dendritic cell growth that was recently described for mouse blood now has been modified to MHC class II-negative precursors in marrow. A key step is to remove the majority of nonadherent, newly formed granulocytes by gentle washes during the first 2-4 d of culture. This leaves behind proliferating clusters that are loosely attached to a more firmly adherent "stroma." At days 4-6 the clusters can be dislodged, isolated by 1-g sedimentation, and upon reculture, large numbers of dendritic cells are released. The latter are readily identified on the basis of their distinct cell shape, ultrastructure, and repertoire of antigens, as detected with a panel of monoclonal antibodies. The dendritic cells express high levels of MHC class II products and act as powerful accessory cells for initiating the mixed leukocyte reaction. Neither the clusters nor mature dendritic cells are generated if macrophage colony-stimulating factor rather than granulocyte/macrophage colony-stimulating factor (GM-CSF) is applied. Therefore, GM-CSF generates all three lineages of myeloid cells (granulocytes, macrophages, and dendritic cells). Since > 5 x 10(6) dendritic cells develop in 1 wk from precursors within the large hind limb bones of a single animal, marrow progenitors can act as a major source of dendritic cells. This feature should prove useful for future molecular and clinical studies of this otherwise trace cell type.

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15

Brinker, Karen G., Emily Martin, Paul Borron, Elahe Mostaghel, Carolyn Doyle, Clifford V. Harding, and Jo Rae Wright. "Surfactant protein D enhances bacterial antigen presentation by bone marrow-derived dendritic cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 6 (December 1, 2001): L1453—L1463. http://dx.doi.org/10.1152/ajplung.2001.281.6.l1453.

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Surfactant protein (SP) D functions as a soluble pattern recognition molecule to mediate the clearance of pathogens by phagocytes in the innate immune response. We hypothesize that SP-D may also interact with dendritic cells, the most potent antigen presenting cell, to enhance uptake and presentation of bacterial antigens. Using mouse bone marrow-derived dendritic cells, we show that SP-D binds to immature dendritic cells in a dose-, carbohydrate-, and calcium-dependent manner, whereas SP-D binding to mature dendritic cells is reduced. SP-D also binds to Escherichia coli HB101 and enhances its association with dendritic cells. Additionally, SP-D enhances the antigen presentation of an ovalbumin fusion protein expressed in E. coli HB101 to ovalbumin-specific major histocompatibility complex class II T cell hybridomas. The enhancement of antigen presentation by SP-D is dose dependent and is not shared by other collectin-like proteins tested. These studies demonstrate that SP-D augments antigen presentation by dendritic cells and suggest that innate immune molecules such as SP-D may help initiate an adaptive immune response for the purpose of resolving an infection.

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16

Vassiliou, Evros, Vikas Sharma, Huie Jing, Farzad Sheibanie, and Doina Ganea. "Prostaglandin E2Promotes the Survival of Bone Marrow-Derived Dendritic Cells." Journal of Immunology 173, no. 11 (November 19, 2004): 6955–64. http://dx.doi.org/10.4049/jimmunol.173.11.6955.

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17

Wang, Jing, Xiaomin Dai, Chiaching Hsu, Changsheng Ming, Ying He, Ji Zhang, Lai Wei, et al. "Discrimination of the heterogeneity of bone marrow-derived dendritic cells." Molecular Medicine Reports 16, no. 5 (May 2017): 6787–93. http://dx.doi.org/10.3892/mmr.2017.7448.

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18

Jin, Cheng-Yun, Min-Ho Han, Cheol Park, Hye-Jin Hwang, Eun-A. Choi, and Yung-Hyun Choi. "Sarijang Enhances Maturation of Murine Bone Marrow-Derived Dendritic Cells." Journal of Life Science 21, no. 12 (December 31, 2011): 1789–94. http://dx.doi.org/10.5352/jls.2011.21.12.1789.

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19

Williams, Natasha L., Eveline Kloeze, Brenda L. Govan, Heinrich Käorner, and Natkunam Ketheesan. "Burkholderia pseudomallei enhances maturation of bone marrow-derived dendritic cells." Transactions of the Royal Society of Tropical Medicine and Hygiene 102 (December 2008): S71—S75. http://dx.doi.org/10.1016/s0035-9203(08)70019-1.

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20

Nikolic, T. "Developmental stages of myeloid dendritic cells in mouse bone marrow." International Immunology 15, no. 4 (April 1, 2003): 515–24. http://dx.doi.org/10.1093/intimm/dxg050.

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21

Wu, Zhiguang, Lisa Rothwell, John R. Young, Jim Kaufman, Colin Butter, and Pete Kaiser. "Generation and characterization of chicken bone marrow‐derived dendritic cells." Immunology 129, no. 1 (December 8, 2009): 133–45. http://dx.doi.org/10.1111/j.1365-2567.2009.03129.x.

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22

Bonham, C. Andrew, Lina Lu, Youping Li, Rosemary A. Hoffman, Richard L. Simmons, and Angus W. Thomson. "NITRIC OXIDE PRODUCTION BY MOUSE BONE MARROW-DERIVED DENDRITIC CELLS." Transplantation 62, no. 12 (December 1996): 1871–77. http://dx.doi.org/10.1097/00007890-199612270-00033.

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23

Feili-Hariri, M., X. Dong, S. M. Alber, S. C. Watkins, R. D. Salter, and P. A. Morel. "Immunotherapy of NOD mice with bone marrow-derived dendritic cells." Diabetes 48, no. 12 (December 1, 1999): 2300–2308. http://dx.doi.org/10.2337/diabetes.48.12.2300.

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24

Zhang, Jingzhu, Teerawit Supakorndej, Joseph R. Krambs, Mahil Rao, Grazia Abou-Ezzi, Rachel Y. Ye, Sidan Li, Kathryn Trinkaus, and Daniel C. Link. "Bone marrow dendritic cells regulate hematopoietic stem/progenitor cell trafficking." Journal of Clinical Investigation 129, no. 7 (June 10, 2019): 2920–31. http://dx.doi.org/10.1172/jci124829.

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25

Creusot, Rémi J., Shahriar S. Yaghoubi, Pearl Chang, Justine Chia, Christopher H. Contag, Sanjiv S. Gambhir, and C. Garrison Fathman. "Lymphoid tissue–specific homing of bone marrow–derived dendritic cells." Blood 113, no. 26 (June 25, 2009): 6638–47. http://dx.doi.org/10.1182/blood-2009-02-204321.

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Abstract Because of their potent immunoregulatory capacity, dendritic cells (DCs) have been exploited as therapeutic tools to boost immune responses against tumors or pathogens, or dampen autoimmune or allergic responses. Murine bone marrow–derived DCs (BM-DCs) are the closest known equivalent of the blood monocyte-derived DCs that have been used for human therapy. Current imaging methods have proven unable to properly address the migration of injected DCs to small and deep tissues in mice and humans. This study presents the first extensive analysis of BM-DC homing to lymph nodes (and other selected tissues) after intravenous and intraperitoneal inoculation. After intravenous delivery, DCs accumulated in the spleen, and preferentially in the pancreatic and lung-draining lymph nodes. In contrast, DCs injected intraperitoneally were found predominantly in peritoneal lymph nodes (pancreatic in particular), and in omentum-associated lymphoid tissue. This uneven distribution of BM-DCs, independent of the mouse strain and also observed within pancreatic lymph nodes, resulted in the uneven induction of immune response in different lymphoid tissues. These data have important implications for the design of systemic cellular therapy with DCs, and in particular underlie a previously unsuspected potential for specific treatment of diseases such as autoimmune diabetes and pancreatic cancer.

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Kim, Mi-Hyoung, and Hong-Gu Joo. "Immunostimulatory effects of fucoidan on bone marrow-derived dendritic cells." Immunology Letters 115, no. 2 (January 2008): 138–43. http://dx.doi.org/10.1016/j.imlet.2007.10.016.

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27

Young, J. W., P. Szabolcs, and M. A. Moore. "Identification of dendritic cell colony-forming units among normal human CD34+ bone marrow progenitors that are expanded by c-kit-ligand and yield pure dendritic cell colonies in the presence of granulocyte/macrophage colony-stimulating factor and tumor necrosis factor alpha." Journal of Experimental Medicine 182, no. 4 (October 1, 1995): 1111–19. http://dx.doi.org/10.1084/jem.182.4.1111.

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Several cytokines, especially granulocyte/macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha), have been identified that foster the development of dendritic cells from blood and bone marrow precursors in suspension cultures. These precursors are reported to be infrequent or to yield small numbers of dendritic cells in colony-forming assays. Here we readily identify dendritic cell colony-forming units (CFU-DC) that give rise to pure dendritic cell colonies. Human CD34+ bone marrow progenitors were expanded in semi-solid cultures with serum-replete medium containing c-kit-ligand, GM-CSF, and TNF-alpha. The addition of TNF-alpha to GM-CSF did not alter the number of typical GM colonies but did generate pure dendritic cell colonies that accounted for approximately 40% of the total colony growth. When the two distinct types of colonies were plucked from methylcellulose and tested for T cell-stimulatory activity in the mixed leukocyte reaction, the potency of colony-derived dendritic cells exceeded that of CFU-GM progeny from the same cultures by at least 1.5-2 logs. Immunophenotyping and cytochemical staining of the CFU-DC-derived progeny was also characteristic of dendritic cells. Other myeloid cells were not identified in these colonies. The addition of c-kit-ligand to GM-CSF- and TNF-alpha-supplemented suspensions of CD34+ bone marrow cells expanded CFU-DCs almost 100-fold by 14 d. We conclude that normal human CD34+ bone marrow cells include substantial numbers of clonogenic progenitors, distinct from CFU-GMs, that can give rise to pure dendritic cell colonies. These CFU-DCs can be expanded for several weeks by in vitro culture with c-kit-ligand, and their differentiation requires exogenous TNF-alpha in addition to GM-CSF. We speculate that this dendritic cell-committed pathway may in the steady state contribute cells to the epidermis and afferent lymph, where dendritic cells are the principal myeloid cell type, and may increase the numbers of these specialized antigen-presenting cells during T cell-mediated immune responses.

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28

Liau, Linda M., Keith L. Black, Robert M. Prins, Steven N. Sykes, Pier-Luigi DiPatre, Timothy F. Cloughesy, Donald P. Becker, and Jeff M. Bronstein. "Treatment of intracranial gliomas with bone marrow—derived dendritic cells pulsed with tumor antigens." Journal of Neurosurgery 90, no. 6 (June 1999): 1115–24. http://dx.doi.org/10.3171/jns.1999.90.6.1115.

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Object. An approach toward the treatment of intracranial gliomas was developed in a rat experimental model. The authors investigated the ability of “professional” antigen-presenting cells (dendritic cells) to enhance host antitumor immune responses when injected as a vaccine into tumor-bearing animals.Methods. Dendritic cells, the most potent antigen-presenting cells in the body, were isolated from rat bone marrow precursors stimulated in vitro with granulocyte—macrophage colony-stimulating factor (GM-CSF) and interleukin-4. Cultured cell populations were confirmed to be functional antigen-presenting cells on the basis of expressed major histocompatibility molecules, as analyzed by fluorescence-activated cell sorter cytofluorography. These dendritic cells were then pulsed (cocultured) ex vivo with acid-eluted tumor antigens from 9L glioma cells. Thirty-eight adult female Fischer 344 rats harboring 7-day-old intracranial 9L tumors were treated with three weekly subcutaneous injections of either control media (10 animals), unpulsed dendritic cells (six animals), dendritic cells pulsed with peptides extracted from normal rat astrocytes (10 animals), or 9L tumor antigen—pulsed dendritic cells (12 animals). The animals were followed for survival. At necropsy, the rat brains were removed and examined histologically, and spleens were harvested for cell-mediated cytotoxicity assays.The results indicate that tumor peptide-pulsed dendritic cell therapy led to prolonged survival in rats with established intracranial 9L tumors implanted 7 days prior to the initiation of vaccine therapy in vivo. Immunohistochemical analyses were used to document a significantly increased perilesional and intratumoral infiltration of CD8+ and CD4+ T cells in the groups treated with tumor antigen—pulsed dendritic cells compared with the control groups. In addition, the results of in vitro cytotoxicity assays suggest that vaccination with these peptide-pulsed dendritic cells can induce specific cytotoxic T lymphocytes against 9L tumor cells.Conclusions. Based on these results, dendritic antigen-presenting cells pulsed with acid-eluted peptides derived from autologous tumors represent a promising approach to the immunotherapy of established intracranial gliomas, which may serve as a basis for designing clinical trials in patients with brain tumors.

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29

Kraal, G., M. Breel, M. Janse, and G. Bruin. "Langerhans' cells, veiled cells, and interdigitating cells in the mouse recognized by a monoclonal antibody." Journal of Experimental Medicine 163, no. 4 (April 1, 1986): 981–97. http://dx.doi.org/10.1084/jem.163.4.981.

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An mAb, NLDC-145, is described that specifically reacts with a group of nonlymphoid dendritic cells including Langerhans cells (LC), veiled cells (VC), and interdigitating cells (IDC). The antibody does not react with precursor cells in bone marrow and blood. Macrophages are not stained by the antibody, but a subpopulation of Ia+ peritoneal exudate cells is recognized. Possible relationships of the various nonlymphoid dendritic cell (NLDC) types are discussed.

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30

Garrigan, K., P. Moroni-Rawson, C. McMurray, I. Hermans, N. Abernethy, J. Watson, and F. Ronchese. "Functional comparison of spleen dendritic cells and dendritic cells cultured in vitro from bone marrow precursors." Blood 88, no. 9 (November 1, 1996): 3508–12. http://dx.doi.org/10.1182/blood.v88.9.3508.bloodjournal8893508.

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We have compared dendritic cells (DC) isolated from mouse spleen, or generated in vitro from bone marrow (BM) precursors cultured in granulocyte macrophage-colony stimulating factor (GM-CSF) and interleukin-4 (IL-4), for the ability to process and present soluble antigen and stimulate major histocompatibility complex (MHC) Class II-restricted T cells. DC from spleen or BM cultures were equally able to stimulate the in vitro proliferation of allogeneic T cells or of antigen-specific T-cell receptor (TCR)-transgenic T cells. Both DC populations also induced comparable levels of IL-2 secretion by a T-cell hybridoma. Therefore, splenic and BM-derived DC express comparable levels of (Antigen + MHC Class II) ligands and/or costimulatory molecules and have comparable ability to stimulate T-cell responses. When presentation of a native protein antigen, rather than peptide, was evaluated, BM-derived DC were at least 50 times better than splenic DC at stimulating the proliferation of TCR-transgenic T cells. The antigen processing ability of the two populations was similar only when splenic DC were used immediately ex vivo. Therefore, unlike spleen DC, BM-derived DC maintain the capacity to process protein antigen for MHC Class II presentation during in vitro culture. Due to these characteristics, BM-derived DC may represent a useful tool in immunotherapy studies, as they combine high T-cell stimulatory properties with the capacity to process and present native antigen.

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Montagna, Daniela, Rita Maccario, Franco Locatelli, Vittorio Rosti, Young Yang, Peggy Farness, Antonia Moretta, Patrizia Comoli, Enrica Montini, and Antonella Vitiello. "Ex vivo priming for long-term maintenance of antileukemia human cytotoxic T cells suggests a general procedure for adoptive immunotherapy." Blood 98, no. 12 (December 1, 2001): 3359–66. http://dx.doi.org/10.1182/blood.v98.12.3359.

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Abstract Adoptive cellular immunotherapy has proven to be a successful approach in preventing and curing cytomegalovirus infection and Epstein-Barr virus–associated lymphomas after bone marrow transplantation. Translation of this approach for preventing leukemia relapse after bone marrow transplantation might require ex vivo priming and long-term maintenance of leukemia blast-specific T cells. To accomplish this goal, procedures were optimized for the in vitro priming of naive CD8 using dendritic cells activated by CD40 ligation, interleukin-12 (IL-12), and IL-7. Using T lymphocytes and dendritic cells obtained from HLA-matched allogeneic bone marrow transplantation donors and leukemia blasts as a source of tumor antigens, anti–acute myeloid leukemia cytotoxic T lymphocytes (CTLs) were induced. In these experiments, it was found that though it is possible to induce CTLs using immature dendritic cells, IL-12, and IL-7, obtaining long-term CTLs requires the presence of CD4 T cells in the priming phase. Using this approach, long-term antileukemia CTL lines could be generated from 4 of 4 bone marrow donors. Because this procedure does not require definition of the target antigen and because it selects responding cells from a virgin T-cell repertoire, its general application is suggested in adoptive immunotherapy and in the definition of tumor rejection antigens.

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Theisen, Derek, and Kenneth Murphy. "The role of cDC1s in vivo: CD8 T cell priming through cross-presentation." F1000Research 6 (February 1, 2017): 98. http://dx.doi.org/10.12688/f1000research.9997.1.

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The cDC1 subset of classical dendritic cells is specialized for priming CD8 T cell responses through the process of cross-presentation. The molecular mechanisms of cross-presentation remain incompletely understood because of limited biochemical analysis of rare cDC1 cells, difficulty in their genetic manipulation, and reliance onin vitrosystems based on monocyte- and bone-marrow-derived dendritic cells. This review will discuss cross-presentation from the perspective of studies with monocyte- or bone-marrow-derived dendritic cells while highlighting the need for future work examining cDC1 cells. We then discuss the role of cDC1s as a cellular platform to combine antigen processing for class I and class II MHC presentation to allow the integration of “help” from CD4 T cells during priming of CD8 T cell responses.

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33

Li, Jian-Ming, Wayne Harris, Ebenezer David, Sagar Lonial, and Ned Waller. "Donor Dendritic Cells Regulate Immune Reconstitution after Allogeneic Bone Marrow Transplantation." Blood 104, no. 11 (November 16, 2004): 3073. http://dx.doi.org/10.1182/blood.v104.11.3073.3073.

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Abstract Background: Infection, graft versus host disease (GVHD) and leukemia relapse following allogeneic bone marrow transplantation (BMT) represent complications due to impaired or inappropriate immune reconstitution. Clinical data indicate that donor type 2 dendritic cells (DC) may inhibit graft-versus-leukemia effects and chronic GVHD following allogeneic BMT from HLA matched siblings (Waller et al. Blood 2001 97:2948) and more rapid recovery of lymphocytes, γ δ - T-cells, and dendritic cells is associated with improved post-transplant relapse-free survival. We developed a murine BMT model to test the hypothesis that donor DC regulate immune reconstitution following BMT. B10BR [H-2kk] recipients transplanted with CD11b-depleted donor BM cells and purified Thy 1.1+ congenic spleen T-cells from C57BL/6 [H-2kb] donors had markedly enhanced expansion of donor Thy 1.1+ T-cells and leukemia-free survival (50%) compared to recipients of donor T-cells plus un-manipulated BM (0% survival; Li and Waller BBMT 2004 10:540). In this report we investigated whether FACS purified donor BM DC subsets would interact with donor T-cells to regulate post-transplant immune reconstitution after MHC mis-matched BMT. Methods: B10.BR mice were lethally irradiated then transplanted with 5,000 FACS sorted Lin− sca-1+ c-kit+ C57BL/6 hematopoietic progenitor cells, 300,000 Thy 1.1+ C57BL/6 T-cells and 50,000 of either CD11b+ or CD11b− BM DC subsets (lin− CD11c+). Control mice received donor T-cells and 5 x 106 un-manipulated BM containing an equivalent number of donor HPC and DC. Engraftment and chimerism were assessed by FACS analysis of peripheral blood and BM. RT PCR measured levels of transcription factors in the BM at the time of hematopoietic engraftment. Results: Equivalent survival (60%) was seen among recipients of FACS purified donor T-cells combined with FACS purified HPC alone, HPC plus CD11b+ and HPC plus CD11b− DC. Recipients of HPC, T-cells, plus CD11b+ donor DC showed a large expansion of donor-spleen derived Thy 1.1+ regulatory T-cells (Treg, CD3+ CD4+ CD25+ CD69−) at day +10, mixed chimerism, and markedly suppressed levels of donor Thy 1.1+ T-cell engraftment at day +60 post-transplant compared to recipients of HPC plus T-cells. Recipients of HPC, T-cells and CD11b− DC had few donor Treg at day +10, more donor CD11b− blood DC, and full donor chimerism, with subsequent expansion of donor-derived T-cells over the next 2 months without developing significant GVHD. T-cell receptor (TCR) phenotyping demonstrated higher numbers of donor Thy 1.1+γ δ - T-cells at day +30 and +60 among recipients of CD11b− DC. RT PCR of mRNA from day +10 BM shows enhanced levels of Th1/Tc1 associated transcription factors JAK1, JAK2, Stat1, Stat 4 and TYK2 among transplant recipients that received FACS purified HPC, CD11b− DC and T-cells compared to recipients of HPC, CD11b+ DC and T-cells. Conclusion: Using highly purified fractions of donor HPC, DC, and T-cells, we demonstrate a novel and significant immune-inhibitory effect of donor CD11b+ DC on post-transplant immune reconstitution. In contrast, enhanced immune reconstitution was observed among recipients of FACS purified CD11b− donor DC compared to grafts containing only HPC and FACS sorted donor T-cells. These data are consistent with a model of indirect allo-antigen presentation by donor DC to donor T-cells in the first days post-transplant leading to stable DC-polarization of donor T-cells that affects long-term post-transplant immune reconstitution and leukemia-free survival.

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Szabolcs, Paul, H. F. Gallardo, David H. Ciocon, Michel Sadelain, and James W. Young. "Retrovirally Transduced Human Dendritic Cells Express a Normal Phenotype and Potent T-Cell Stimulatory Capacity." Blood 90, no. 6 (September 15, 1997): 2160–67. http://dx.doi.org/10.1182/blood.v90.6.2160.

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Abstract Dendritic cells are attractive candidates for vaccine-based immunotherapy because of their potential to function as natural adjuvants for poorly immunogenic proteins derived from tumors or microbes. In this study, we evaluated the feasibility and consequences of introducing foreign genetic material by retroviral vectors into dendritic cell progenitors. Proliferating human bone marrow and cord blood CD34+ cells were infected by retroviral vectors encoding the murine CD2 surface antigen. Mean transduction efficiency in dendritic cells was 11.5% from bone marrow and 21.2% from cord blood progenitors. Transduced or untransduced dendritic cell progeny expressed comparable levels of HLA-DR, CD83, CD1a, CD80, CD86, S100, and p55 antigens. Granulocytes, macrophages, and dendritic cells were equally represented among the transduced and mock-transduced cells, thus showing no apparent alteration in the differentiation of transduced CD34+ precursors. The T-cell stimulatory capacity of retrovirally modified and purified mCD2-positive allogeneic or nominal antigen-pulsed autologous dendritic cells was comparable with that of untransduced dendritic cells. Human CD34+ dendritic cell progenitors can therefore be efficiently transduced using retroviral vectors and can differentiate into potent immunostimulatory dendritic cells without compromising their T-cell stimulatory capacity or the expression of critical costimulatory molecules and phenotypic markers. These results support ongoing efforts to develop genetically modified dendritic cells for immunotherapy.

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Iversen, Per Ole, Nils Hjeltnes, Bjørn Holm, Torun Flatebø, Inger Strøm-Gundersen, Wenche Rønning, Johan Stanghelle, and Haakon B. Benestad. "Depressed immunity and impaired proliferation of hematopoietic progenitor cells in patients with complete spinal cord injury." Blood 96, no. 6 (September 15, 2000): 2081–83. http://dx.doi.org/10.1182/blood.v96.6.2081.h8002081_2081_2083.

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The bone marrow is supplied with both sensory and autonomic neurons, but their roles in regulating hematopoietic and immunocompetent cells are unknown. Leukocyte growth and activity in patients with stable and complete spinal cord injuries were studied. The innervation of the bone marrow below the injury level lacked normal supraspinal activity, that is, a decentralized bone marrow. Lymphocyte functions were markedly decreased in injured patients. Long-term colony formation of all hematopoietic cell lineages, including dendritic cells, by decentralized bone marrow cells was substantially reduced. It was concluded that nonspecific and adaptive lymphocyte-mediated immunity and growth of early hematopoietic progenitor cells are impaired in patients with spinal cord injuries. Possibly, this reflects cellular defects caused by the malfunctioning neuronal regulation of immune and bone marrow function.

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Drakes, Maureen, Thomas Blanchard, and Steven Czinn. "Bacterial Probiotic Modulation of Dendritic Cells." Infection and Immunity 72, no. 6 (June 2004): 3299–309. http://dx.doi.org/10.1128/iai.72.6.3299-3309.2004.

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ABSTRACT Intestinal dendritic cells are continually exposed to ingested microorganisms and high concentrations of endogenous bacterial flora. These cells can be activated by infectious agents and other stimuli to induce T-cell responses and to produce chemokines which recruit other cells to the local environment. Bacterial probiotics are of increasing use against intestinal disorders such as inflammatory bowel disease. They act as nonpathogenic stimuli within the gut to regain immunologic quiescence. This study was designed to determine the ability of a bacterial probiotic cocktail VSL#3 to alter cell surface antigen expression and cytokine production in bone marrow-derived dendritic cell-enriched populations. Cell surface phenotype was monitored by monoclonal fluorescent antibody staining, and cytokine levels were quantitated by enzyme-linked immunosorbent assay. High-dose probiotic upregulated the expression of C80, CD86, CD40, and major histocompatibility complex class II I-Ad. Neither B7-DC or B7RP-1 was augmented after low-dose probiotic or Lactobacillus casei treatment, but B7RP-1 showed increased expression on dendritic cells stimulated with the gram-negative bacterium Escherichia coli. Functional studies showed that probiotic did not enhance the ability of dendritic cells to induce allogeneic T-cell proliferation, as was observed for E. coli. Substantial enhancement of interleukin-10 release was observed in dendritic cell-enriched culture supernatants after 3 days of probiotic stimulation. These results demonstrate that probiotics possess the ability to modulate dendritic cell surface phenotype and cytokine release in granulocyte-macrophage colony-stimulating factor-stimulated bone marrow-derived dendritic cells. Regulation of dendritic cell cytokines by probiotics may contribute to the benefit of these molecules in treatment of intestinal diseases.

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37

Bénard, Alan, Jérôme Boué, Emmanuelle Chapey, Martial Jaume, Bruno Gomes, and Gilles Dietrich. "Delta opioid receptors mediate chemotaxis in bone marrow-derived dendritic cells." Journal of Neuroimmunology 197, no. 1 (June 2008): 21–28. http://dx.doi.org/10.1016/j.jneuroim.2008.03.020.

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Fogg, D. K. "A Clonogenic Bone Marrow Progenitor Specific for Macrophages and Dendritic Cells." Science 311, no. 5757 (January 6, 2006): 83–87. http://dx.doi.org/10.1126/science.1117729.

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39

Ricklin Gutzwiller, Meret Elisabeth, Hervé Raphaël Moulin, Andreas Zurbriggen, Petra Roosje, and Artur Summerfield. "Comparative analysis of canine monocyte- and bone-marrow-derived dendritic cells." Veterinary Research 41, no. 4 (February 22, 2010): 40. http://dx.doi.org/10.1051/vetres/2010012.

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40

ILIC, N., M. COLIC, A. GRUDEN-MOVSESIJAN, I. MAJSTOROVIC, S. VASILEV, and LJ SOFRONIC-MILOSAVLJEVIC. "Characterization of rat bone marrow dendritic cells initially primed byTrichinella spiralisantigens." Parasite Immunology 30, no. 9 (September 2008): 491–95. http://dx.doi.org/10.1111/j.1365-3024.2008.01049.x.

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41

Latchumanan, Vinoth K., Balwan Singh, Pawan Sharma, and Krishnamurthy Natarajan. "Mycobacterium tuberculosisAntigens Induce the Differentiation of Dendritic Cells from Bone Marrow." Journal of Immunology 169, no. 12 (December 15, 2002): 6856–64. http://dx.doi.org/10.4049/jimmunol.169.12.6856.

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42

Bennett, Clare L., Ana Misslitz, Lisa Colledge, Toni Aebischer, and C. Clare Blackburn. "Silent infection of bone marrow-derived dendritic cells byLeishmania mexicana amastigotes." European Journal of Immunology 31, no. 3 (March 2001): 876–83. http://dx.doi.org/10.1002/1521-4141(200103)31:3<876::aid-immu876>3.0.co;2-i.

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43

Wu, Tingting, Yan Qi, Dan Zhang, Qingle Song, Conglian Yang, Xiaomeng Hu, Yuling Bao, Yongdan Zhao, and Zhiping Zhang. "Bone Marrow Dendritic Cells Derived Microvesicles for Combinational Immunochemotherapy against Tumor." Advanced Functional Materials 27, no. 42 (September 13, 2017): 1703191. http://dx.doi.org/10.1002/adfm.201703191.

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44

Ding, Yingjun, Xiang Cheng, Tingting Tang, Rui Yao, Yong Chen, Jiangjiao Xie, Xian Yu, and Yuhua Liao. "Rapamycin modulates the maturation of rat bone marrow-derived dendritic cells." Journal of Huazhong University of Science and Technology [Medical Sciences] 28, no. 4 (August 2008): 391–95. http://dx.doi.org/10.1007/s11596-008-0405-1.

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Putra, Agus Budiawan Naro, Kosuke Nishi, Ryusuke Shiraishi, Mikiharu Doi, and Takuya Sugahara. "Jellyfish collagen stimulates maturation of mouse bone marrow-derived dendritic cells." Journal of Functional Foods 14 (April 2015): 308–17. http://dx.doi.org/10.1016/j.jff.2015.02.008.

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46

Awasthi, Shanjana, and Jodie Cropper. "Immunophenotype and functions of fetal baboon bone-marrow derived dendritic cells." Cellular Immunology 240, no. 1 (March 2006): 31–40. http://dx.doi.org/10.1016/j.cellimm.2006.06.001.

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47

Liao, H. F., Y. C. Yang, Y. Y. Chen, M. L. Hsu, H. R. Shieh, and Y. J. Chen. "Macrophages derived from bone marrow modulate differentiation of myeloid dendritic cells." Cellular and Molecular Life Sciences 64, no. 1 (December 14, 2006): 104–11. http://dx.doi.org/10.1007/s00018-006-6407-x.

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Yu, Duowei, Yun Sun, Jianqing Wu, and Sheng Yuan. "Cytokines mRNA in bone marrow-derived dendritic cells in asthmatic mouse." Frontiers of Biology in China 1, no. 3 (September 2006): 241–45. http://dx.doi.org/10.1007/s11515-006-0029-4.

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Alnaeeli, Mawadda, and Yen-Tung A. Teng. "Dendritic cells differentiate into osteoclasts in bone marrow microenvironment in vivo." Blood 113, no. 1 (January 1, 2009): 264–65. http://dx.doi.org/10.1182/blood-2008-09-180836.

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Himoudi, Nourredine, Stephen Nabarro, Jo Buddle, Ayad Eddaoudi, Adrian J. Thrasher, and John Anderson. "Bone Marrow-Derived IFN-Producing Killer Dendritic Cells Account for the Tumoricidal Activity of Unpulsed Dendritic Cells." Journal of Immunology 181, no. 9 (October 20, 2008): 6654–63. http://dx.doi.org/10.4049/jimmunol.181.9.6654.

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