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Journal articles on the topic 'Human dendritic cell'

Author: Grafiati

Published: 11 March 2023

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1

Bigley, Venetia, Urszula Cytlak, and Matthew Collin. "Human dendritic cell immunodeficiencies." Seminars in Cell & Developmental Biology 86 (February 2019): 50–61. http://dx.doi.org/10.1016/j.semcdb.2018.02.020.

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2

Collin, Matthew, Naomi McGovern, and Muzlifah Haniffa. "Human dendritic cell subsets." Immunology 140, no. 1 (August 12, 2013): 22–30. http://dx.doi.org/10.1111/imm.12117.

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3

Tsunoda, Rikiya, Alain Bosseloir, Kikuo Onozaki, Ernst Heinen, Katsuya Miyake, Hiro-oki Okamura, Kazunori Suzuki, Teizou Fujita, Léon J. Simar, and Naonori Sugai. "Human follicular dendritic cells in vitro and follicular dendritic-cell-like cells." Cell and Tissue Research 288, no. 2 (April 9, 1997): 381–89. http://dx.doi.org/10.1007/s004410050824.

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4

Caron, Gersende, Yves Delneste, Edith Roelandts, Catherine Duez, Jean-Yves Bonnefoy, Joel Pestel, and Pascale Jeannin. "Histamine Polarizes Human Dendritic Cells into Th2 Cell-Promoting Effector Dendritic Cells." Journal of Immunology 167, no. 7 (October 1, 2001): 3682–86. http://dx.doi.org/10.4049/jimmunol.167.7.3682.

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5

Olweus, J., A. BitMansour, R. Warnke, P. A. Thompson, J. Carballido, L. J. Picker, and F. Lund-Johansen. "Dendritic cell ontogeny: A human dendritic cell lineage of myeloid origin." Proceedings of the National Academy of Sciences 94, no. 23 (November 11, 1997): 12551–56. http://dx.doi.org/10.1073/pnas.94.23.12551.

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6

Foster, Barbara, Dean D. Metcalfe, and Calman Prussin. "Human dendritic cell 1 and dendritic cell 2 subsets express FcεRI." Journal of Allergy and Clinical Immunology 112, no. 6 (December 2003): 1132–38. http://dx.doi.org/10.1016/j.jaci.2003.09.011.

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7

Lin, Chin-Hsien, Hsun Li, Yi-Nan Lee, Ying-Ju Cheng, Ruey-Meei Wu, and Cheng-Ting Chien. "Lrrk regulates the dynamic profile of dendritic Golgi outposts through the golgin Lava lamp." Journal of Cell Biology 210, no. 3 (July 27, 2015): 471–83. http://dx.doi.org/10.1083/jcb.201411033.

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Constructing the dendritic arbor of neurons requires dynamic movements of Golgi outposts (GOPs), the prominent component in the dendritic secretory pathway. GOPs move toward dendritic ends (anterograde) or cell bodies (retrograde), whereas most of them remain stationary. Here, we show that Leucine-rich repeat kinase (Lrrk), the Drosophila melanogaster homologue of Parkinson’s disease–associated Lrrk2, regulates GOP dynamics in dendrites. Lrrk localized at stationary GOPs in dendrites and suppressed GOP movement. In Lrrk loss-of-function mutants, anterograde movement of GOPs was enhanced, whereas Lrrk overexpression increased the pool size of stationary GOPs. Lrrk interacted with the golgin Lava lamp and inhibited the interaction between Lva and dynein heavy chain, thus disrupting the recruitment of dynein to Golgi membranes. Whereas overexpression of kinase-dead Lrrk caused dominant-negative effects on GOP dynamics, overexpression of the human LRRK2 mutant G2019S with augmented kinase activity promoted retrograde movement. Our study reveals a pathogenic pathway for LRRK2 mutations causing dendrite degeneration.

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Elahi, Zahra, Paul W. Angel, Suzanne K. Butcher, Nadia Rajab, Jarny Choi, Yidi Deng, Justine D. Mintern, Kristen Radford, and Christine A. Wells. "The Human Dendritic Cell Atlas: An Integrated Transcriptional Tool to Study Human Dendritic Cell Biology." Journal of Immunology 209, no. 12 (December 15, 2022): 2352–61. http://dx.doi.org/10.4049/jimmunol.2200366.

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Abstract Dendritic cells (DCs) are functionally diverse and are present in most adult tissues, but deep understanding of human DC biology is hampered by relatively small numbers of these in circulation and their short lifespan in human tissues. We built a transcriptional atlas of human DCs by combining samples from 14 expression profiling studies derived from 10 laboratories. We identified significant gene expression variation of DC subset–defining markers across tissue type and upon viral or bacterial stimulation. We further highlight critical gaps between in vitro–derived DC subsets and their in vivo counterparts and provide evidence that monocytes or cord blood progenitor in vitro–differentiated DCs fail to capture the repertoire of primary DC subsets or behaviors. In constructing a reference DC atlas, we provide an important resource for the community wishing to identify and annotate tissue-specific DC subsets from single-cell datasets, or benchmark new in vitro models of DC biology.

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9

Newman, Rosie, Raina Simpson, Teresa Domagala, Mei Lim, Linda Crofts, Glenn Pilkington, and Denese Marks. "Generation of Dendritic Cells from Human Cell Expressed Cytokines." Blood 108, no. 11 (November 16, 2006): 5208. http://dx.doi.org/10.1182/blood.v108.11.5208.5208.

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Abstract Traditionally, human cytokines have been expressed in non-human cells, including bacteria, yeast and mouse cells. However, the biological importance of species-specific post-translational modifications, in particular glycosylation, is increasingly being implicated as pivotal to protein function. Glycosylation is important for solubility, resistance to proteolysis, immunogenicity, biological recognition, biological activity, in vivo stability and clearance of glycoproteins including cytokines and growth factors, as up to 75% of their mass may consist of carbohydrate moieties. Clinical trials in cancer immunotherapy have attempted to benefit from the ability of autologous dendritic cells to boost antigen specific T-cell immunity. To date most clinical trials have generated dendritic cells using cytokines expressed in non-human cells. We have purified recombinant human cytokines expressed in modified human 293 cells. Human cell expressed human cytokines including IL-4, GM-CSF and TNF-alpha were used to generate dendritic cells from human peripheral blood mononuclear cells. The resulting cells exhibited a typical mature dendritic cell phenotype including expression of CD209, HLA-DR, CD40, CD80, CD83 and CD86, and were able to generate a T-cell response. In vitro comparisons of the biological activity of human cell expressed cytokines, in particular IL-4, with those expressed in other species has demonstrated that human cell expressed cytokines are more stable. It is proposed that the enhanced biological stability of human cytokines derived from a human cell expression system would make these cytokines ideal for ex vivo derivation of immune cells such as dendritic cells for cancer therapy.

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10

Bamboat, Zubin M., Jennifer A. Stableford, George Plitas, Bryan M. Burt, Hoang M. Nguyen, Alexander P. Welles, Mithat Gonen, James W. Young, and Ronald P. DeMatteo. "Human Liver Dendritic Cells Promote T Cell Hyporesponsiveness." Journal of Immunology 182, no. 4 (February 6, 2009): 1901–11. http://dx.doi.org/10.4049/jimmunol.0803404.

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11

Clark, Georgina J., Pablo A. Silveira, P. Mark Hogarth, and Derek N. J. Hart. "The cell surface phenotype of human dendritic cells." Seminars in Cell & Developmental Biology 86 (February 2019): 3–14. http://dx.doi.org/10.1016/j.semcdb.2018.02.013.

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12

Segura, Elodie, Maxime Touzot, Armelle Bohineust, Antonio Cappuccio, Gilles Chiocchia, Anne Hosmalin, Marc Dalod, Vassili Soumelis, and Sebastian Amigorena. "Human Inflammatory Dendritic Cells Induce Th17 Cell Differentiation." Immunity 38, no. 2 (February 2013): 336–48. http://dx.doi.org/10.1016/j.immuni.2012.10.018.

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13

Cabral, M. Guadalupe, A. Rita Piteira, Zélia Silva, Dário Ligeiro, Reinhard Brossmer, and Paula A. Videira. "Human dendritic cells contain cell surface sialyltransferase activity." Immunology Letters 131, no. 1 (June 2010): 89–96. http://dx.doi.org/10.1016/j.imlet.2010.02.009.

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14

Ismaili, Jamila, Véronique Olislagers, Rémy Poupot, Jean-Jacques Fournié, and Michel Goldman. "Human γδ T Cells Induce Dendritic Cell Maturation." Clinical Immunology 103, no. 3 (June 2002): 296–302. http://dx.doi.org/10.1006/clim.2002.5218.

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15

Thurnher, Martin, Christian Radmayr, Reinhold Ramoner, Susanne Ebner, Günther Böck, Helmut Klocker, Nikolaus Romani, and Georg Bartsch. "Human renal-cell carcinoma tissue contains dendritic cells." International Journal of Cancer 68, no. 1 (September 27, 1996): 1–7. http://dx.doi.org/10.1002/(sici)1097-0215(19960927)68:1<1::aid-ijc1>3.0.co;2-v.

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16

Hambleton, Sophie, Sandra Salem, Jacinta Bustamante, Venetia Bigley, Stéphanie Boisson-Dupuis, Joana Azevedo, Anny Fortin, et al. "IRF8Mutations and Human Dendritic-Cell Immunodeficiency." New England Journal of Medicine 365, no. 2 (July 14, 2011): 127–38. http://dx.doi.org/10.1056/nejmoa1100066.

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17

Bachetoni, A., A. D’Ambrosio, P. Mariani, R. Cortesini, and F. Quintieri. "Diltiazem affects human dendritic cell maturation." Transplantation Proceedings 33, no. 1-2 (February 2001): 231–33. http://dx.doi.org/10.1016/s0041-1345(00)01989-8.

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18

Palucka, Karolina, and Jacques Banchereau. "Human dendritic cell subsets in vaccination." Current Opinion in Immunology 25, no. 3 (June 2013): 396–402. http://dx.doi.org/10.1016/j.coi.2013.05.001.

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19

Dubsky, Peter, Hideki Ueno, Bernard Piqueras, John Connolly, Jacques Banchereau, and A. Karolina Palucka. "Human Dendritic Cell Subsets for Vaccination." Journal of Clinical Immunology 25, no. 6 (November 2005): 551–72. http://dx.doi.org/10.1007/s10875-005-8216-7.

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20

Collin, Matthew, and Venetia Bigley. "Human dendritic cell subsets: an update." Immunology 154, no. 1 (February 27, 2018): 3–20. http://dx.doi.org/10.1111/imm.12888.

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21

Shortman, Ken, and Yong-Jun Liu. "Mouse and human dendritic cell subtypes." Nature Reviews Immunology 2, no. 3 (March 2002): 151–61. http://dx.doi.org/10.1038/nri746.

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22

PETERSON, BETH B., and DENNIS M. DACEY. "Morphology of wide-field bistratified and diffuse human retinal ganglion cells." Visual Neuroscience 17, no. 4 (July 2000): 567–78. http://dx.doi.org/10.1017/s0952523800174073.

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To study the detailed morphology of human retinal ganglion cells, we used intracellular injection of horseradish peroxidase and Neurobiotin to label over 1000 cells in an in vitro, wholemount preparation of the human retina. This study reports on the morphology of 119 wide-field bistratified and 42 diffuse ganglion cells. Cells were analyzed quantitatively on the basis of dendritic-field size, soma size, and the extent of dendritic branching. Bistratified cells were similar in dendritic-field diameter (mean ± s.d. = 682 ± 130 μm) and soma diameter (mean ± s.d. = 18 ± 3.3 μm) but showed a broad distribution in the extent of dendritic branching (mean ± s.d. branch point number = 67 ± 32; range = 15–167). Differences in the extent of branching and in dendritic morphology and the pattern of branching suggest that the human retina may contain at least three types of wide-field bistratified cells. Diffuse ganglion cells comprised a largely homogeneous group whose dendrites ramified throughout the inner plexiform layer. The diffuse cells had similar dendritic-field diameters (mean ± s.d. = 486 ± 113 μm), soma diameters (mean ± s.d. = 16 ± 2.3 μm), and branch points numbers (mean ± s.d. = 92 ± 32). The majority had densely branched dendritic trees and thin, very spiny dendrites with many short, fine, twig-like thorny processes. Five of the diffuse cells had much more sparsely branched dendritic trees (<50 branch points) and less spiny dendrites, suggesting that there are possibly two types of diffuse ganglion cells in human retina. Although the presence of a diversity of large bistratified and diffuse ganglion cells has been observed in a variety of mammalian retinas, little is known about the number of cell types, their physiological properties, or their central projections. Some of the human wide-field bistratified cells in the present study, however, show morphological similarities to monkey large bistratified cells that are known to project to the superior colliculus.

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23

PETERSON, BETH B., and DENNIS M. DACEY. "Morphology of wide-field, monostratified ganglion cells of the human retina." Visual Neuroscience 16, no. 1 (January 1999): 107–20. http://dx.doi.org/10.1017/s0952523899161066.

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To determine the number of wide-field, monostratified ganglion cell classes present in the human retina, we analyzed a large sample of ganglion cells by intracellular staining in an in vitro, whole-mount preparation of the retina. Over 1000 cells were labeled by horseradish peroxidase or Neurobiotin; some 200 cells had wide dendritic trees narrowly or broadly stratified within either the inner (ON) or outer (OFF) portion of the inner plexiform layer. Based on dendritic-field size and the pattern and extent of dendritic branching, we have distinguished six wide-field cell groups. The giant very sparse ganglion cells included both inner and outer stratifying cells and were unique both for their extremely large dendritic field (mean diameter = 1077 μm) and extremely sparsely branched dendrites. Four of the cell groups had similarly large dendritic fields, ranging in mean diameter from 737 to 791 μm, but differed in the pattern and extent of dendritic branching, with the number of dendritic branch points ranging from a mean of 33 to 129. Of these four groups, the large very sparse group and the large dense group included both inner and outer stratifying cells, while the large sparse and large moderate groups consisted of inner stratifying cells only. The thorny monostratified ganglion cells were distinct from the other cells in having medium size dendritic fields (mean diameter = 517 μm) and moderately branched, inner stratifying dendritic trees with many thin, spiny, twig-like branchlets. All six groups had medium-size cell bodies, with mean soma diameters ranging from 17 to 21 μm. Though the physiological properties and central projections of human wide-field, monostratified ganglion cells are not known, some of the cells resemble macaque ganglion cells known to project to the lateral geniculate nucleus, the pretectum, or the superior colliculus.

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24

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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25

Zagha, Edward, Satoshi Manita, William N. Ross, and Bernardo Rudy. "Dendritic Kv3.3 Potassium Channels in Cerebellar Purkinje Cells Regulate Generation and Spatial Dynamics of Dendritic Ca2+ Spikes." Journal of Neurophysiology 103, no. 6 (June 2010): 3516–25. http://dx.doi.org/10.1152/jn.00982.2009.

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Purkinje cell dendrites are excitable structures with intrinsic and synaptic conductances contributing to the generation and propagation of electrical activity. Voltage-gated potassium channel subunit Kv3.3 is expressed in the distal dendrites of Purkinje cells. However, the functional relevance of this dendritic distribution is not understood. Moreover, mutations in Kv3.3 cause movement disorders in mice and cerebellar atrophy and ataxia in humans, emphasizing the importance of understanding the role of these channels. In this study, we explore functional implications of this dendritic channel expression and compare Purkinje cell dendritic excitability in wild-type and Kv3.3 knockout mice. We demonstrate enhanced excitability of Purkinje cell dendrites in Kv3.3 knockout mice, despite normal resting membrane properties. Combined data from local application pharmacology, voltage clamp analysis of ionic currents, and assessment of dendritic Ca2+ spike threshold in Purkinje cells suggest a role for Kv3.3 channels in opposing Ca2+ spike initiation. To study the physiological relevance of altered dendritic excitability, we measured [Ca2+]i changes throughout the dendritic tree in response to climbing fiber activation. Ca2+ signals were specifically enhanced in distal dendrites of Kv3.3 knockout Purkinje cells, suggesting a role for dendritic Kv3.3 channels in regulating propagation of electrical activity and Ca2+ influx in distal dendrites. These findings characterize unique roles of Kv3.3 channels in dendrites, with implications for synaptic integration, plasticity, and human disease.

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26

Schmidlin, H., W. Dontje, F. Groot, S. J. Ligthart, A. D. Colantonio, M. E. Oud, E. J. Schilder-Tol, et al. "Stimulated plasmacytoid dendritic cells impair human T-cell development." Blood 108, no. 12 (December 1, 2006): 3792–800. http://dx.doi.org/10.1182/blood-2006-02-004978.

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27

Jesudason, Shilpanjali, Michael G. Collins, Natasha M. Rogers, Svjetlana Kireta, and P. Toby H. Coates. "Non-human primate dendritic cells." Journal of Leukocyte Biology 91, no. 2 (November 28, 2011): 217–28. http://dx.doi.org/10.1189/jlb.0711355.

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28

Van Vré, Emily A., Hidde Bult, Vicky Y. Hoymans, Viggo F. I. Van Tendeloo, Christiaan J. Vrints, and Johan M. Bosmans. "Human C-Reactive Protein Activates Monocyte-Derived Dendritic Cells and Induces Dendritic Cell-Mediated T-Cell Activation." Arteriosclerosis, Thrombosis, and Vascular Biology 28, no. 3 (March 2008): 511–18. http://dx.doi.org/10.1161/atvbaha.107.157016.

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29

Motta, Juliana Maria, Clarissa Rodrigues Nascimento, and Vivian Mary Rumjanek. "Leukemic cell products down-regulate human dendritic cell differentiation." Cancer Immunology, Immunotherapy 59, no. 11 (July 6, 2010): 1645–53. http://dx.doi.org/10.1007/s00262-010-0890-5.

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30

SHNAWA, IBRAHIM M. S. A. W. "Dendritic Cell Based Vaccine for Human Tuberculosis." International Journal of Vaccines and Immune System 2, no. 1 (2017): 01–06. http://dx.doi.org/10.25141/2475-6326-2017-1.0001.

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31

Imai, Fumihiko. "Cluster formation by human peripheral dendritic cell." Japanese Journal of Clinical Immunology 11, no. 2 (1988): 114–20. http://dx.doi.org/10.2177/jsci.11.114.

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32

Ueno, Hideki, Nathalie Schmitt, Eynav Klechevsky, Alexander Pedroza-Gonzalez, Toshimichi Matsui, Gerard Zurawski, SangKon Oh, et al. "Harnessing human dendritic cell subsets for medicine." Immunological Reviews 234, no. 1 (March 2010): 199–212. http://dx.doi.org/10.1111/j.0105-2896.2009.00884.x.

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33

Romani, N., S. Gruner, D. Brang, E. Kämpgen, A. Lenz, B. Trockenbacher, G. Konwalinka, P. O. Fritsch, R. M. Steinman, and G. Schuler. "Proliferating dendritic cell progenitors in human blood." Journal of Experimental Medicine 180, no. 1 (July 1, 1994): 83–93. http://dx.doi.org/10.1084/jem.180.1.83.

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CD34+ cells in human cord blood and marrow are known to give rise to dendritic cells (DC), as well as to other myeloid lineages. CD34+ cells are rare in adult blood, however, making it difficult to use CD34+ cells to ascertain if DC progenitors are present in the circulation and if blood can be a starting point to obtain large numbers of these immunostimulatory antigen-presenting cells for clinical studies. A systematic search for DC progenitors was therefore carried out in several contexts. In each case, we looked initially for the distinctive proliferating aggregates that were described previously in mice. In cord blood, it was only necessary to deplete erythroid progenitors, and add granulocyte/macrophage colony-stimulating factor (GM-CSF) together with tumor necrosis factor (TNF), to observe many aggregates and the production of typical DC progeny. In adult blood from patients receiving CSFs after chemotherapy for malignancy, GM-CSF and TNF likewise generated characteristic DCs from HLA-DR negative precursors. However, in adult blood from healthy donors, the above approaches only generated small DC aggregates which then seemed to become monocytes. When interleukin 4 was used to suppress monocyte development (Jansen, J. H., G.-J. H. M. Wientjens, W. E. Fibbe, R. Willemze, and H. C. Kluin-Nelemans. 1989. J. Exp. Med. 170:577.), the addition of GM-CSF led to the formation of large proliferating DC aggregates and within 5-7 d, many nonproliferating progeny, about 3-8 million cells per 40 ml of blood. The progeny had a characteristic morphology and surface composition (e.g., abundant HLA-DR and accessory molecules for cell-mediated immunity) and were potent stimulators of quiescent T cells. Therefore, large numbers of DCs can be mobilized by specific cytokines from progenitors in the blood stream. These relatively large numbers of DC progeny should facilitate future studies of their Fc epsilon RI and CD4 receptors, and their use in stimulating T cell-mediated resistance to viruses and tumors.

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Yu, Mary Beth, Joshua Guerra, Anthony Firek, and William H. R. Langridge. "Extracellular vimentin modulates human dendritic cell activation." Molecular Immunology 104 (December 2018): 37–46. http://dx.doi.org/10.1016/j.molimm.2018.09.017.

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35

Dallal, Ramsey M., and Michael T. Lotze. "The dendritic cell and human cancer vaccines." Current Opinion in Immunology 12, no. 5 (October 2000): 583–88. http://dx.doi.org/10.1016/s0952-7915(00)00146-1.

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36

Segura, Elodie, and Sebastian Amigorena. "Cross-presentation by human dendritic cell subsets." Immunology Letters 158, no. 1-2 (March 2014): 73–78. http://dx.doi.org/10.1016/j.imlet.2013.12.001.

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37

MacDonald, Kelli P. A., David J. Munster, Georgina J. Clark, Andrzej Dzionek, Juergen Schmitz, and Derek N. J. Hart. "Characterization of human blood dendritic cell subsets." Blood 100, no. 13 (December 15, 2002): 4512–20. http://dx.doi.org/10.1182/blood-2001-11-0097.

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Dendritic cells (DCs) are key antigen-presenting cells for stimulating immune responses and they are now being investigated in clinical settings. Although defined as lineage-negative (Lin−) HLA-DR+ cells, significant heterogeneity in these preparations is apparent, particularly in regard to the inclusion or exclusion of CD14+, CD16+, and CD2+ cells. This study used flow cytometry and a panel of monoclonal antibodies (mAbs), including reagents from the 7th Leukocyte Differentiation Antigen Workshop, to define the cellular composition of 2 standardized peripheral blood mononuclear cell (PBMCs)–derived Lin− HLA-DR+preparations. Lin− cells were prepared from PBMCs by depletion with CD3, CD14, CD19, CD11b, and either CD16 or CD56 mAbs. Analysis of the CD16-replete preparations divided the Lin− HLA-DR+ population into 5 nonoverlapping subsets (mean ± 1 SD): CD123 (mean = 18.3% ± 9.7%), CD1b/c (18.6% ± 7.6%), CD16 (49.6% ± 8.5%), BDCA-3 (2.7% ± 1.4%), and CD34 (5.0% ± 2.4%). The 5 subsets had distinct phenotypes when compared with each other, monocytes, and monocyte-derived DCs (MoDCs). The CD85 family, C-type lectins, costimulatory molecules, and differentiation/activation molecules were also expressed differentially on the 5 Lin−HLA-DR+ subsets, monocytes, and MoDCs. The poor viability of CD123+ DCs in vitro was confirmed, but the CD16+ CD11c+ DC subset also survived poorly. Finally, the individual subsets used as stimulators in allogeneic mixed leukocyte reactions were ranked by their allostimulatory capacity as CD1b/c > CD16 > BDCA-3 > CD123 > CD34. These data provide an opportunity to standardize the DC populations used for future molecular, functional and possibly even therapeutic studies.

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38

Collin, Matthew, Venetia Bigley, Muzlifah Haniffa, and Sophie Hambleton. "Human dendritic cell deficiency: the missing ID?" Nature Reviews Immunology 11, no. 9 (August 19, 2011): 575–83. http://dx.doi.org/10.1038/nri3046.

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39

Rinaldo, C. R. "Dendritic cell-based human immunodeficiency virus vaccine." Journal of Internal Medicine 265, no. 1 (January 2009): 138–58. http://dx.doi.org/10.1111/j.1365-2796.2008.02047.x.

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40

Leylek, Rebecca, Marcela Alcántara-Hernández, Jeffrey M. Granja, Michael Chavez, Kimberly Perez, Oscar R. Diaz, Rui Li, Ansuman T. Satpathy, Howard Y. Chang, and Juliana Idoyaga. "Chromatin Landscape Underpinning Human Dendritic Cell Heterogeneity." Cell Reports 32, no. 12 (September 2020): 108180. http://dx.doi.org/10.1016/j.celrep.2020.108180.

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41

Kaouther, Mnasria, and Oueslati Ridha. "Dendritic Cell-Based Graft Tolerance." ISRN Pharmacology 2011 (April 10, 2011): 1–4. http://dx.doi.org/10.5402/2011/347134.

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It has recently been demonstrated that mouse and human dendritic cells (DCs) can produce IL-2 after activation. However the role of the IL2/IL2R pathway in DC functions has not yet been fully elucidated. The results presented in this study provide several new insights into the role of this pathway in DCs. We report that stimulation of human monocyte-derived DCs with LPS strongly upregulated CD25 (α chain of the IL2R) expression. In additon, by using a humanized monoclonal antibody against CD25, we demonstrated that the IL2 signalling in DC upregulated both IL-12 and γIFN production but decreased IL10 synthesis. We also found that LPS-matured DCs produced IL2. Taken together, these results suggest that IL-2 actively contributes to the DC activation through an autocrine pathway. Furthermore, our results indicate that the IL2 pathway in DC is involved in the development of T-helper priming ability and in the upregulation of surface markers characteristic of a “mature” phenotype. This study therefore provide new molecular clues regarding the split between these two phenomena and unravel new mechanisms of action of anti-CD25 monoclonal antibodies that may contribute to their action in several human immunological disorders such as autoimmune diseases and acute allograft rejection.

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AGRAWAL, A., S. AGRAWAL, and S. GUPTA. "Dendritic cells in human aging." Experimental Gerontology 42, no. 5 (May 2007): 421–26. http://dx.doi.org/10.1016/j.exger.2006.11.007.

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Osada, Takuya, Hirokazu Nagawa, Joji Kitayama, Nelson H. Tsuno, Soichiro Ishihara, Masaru Takamizawa, and Yoichi Shibata. "Peripheral Blood Dendritic Cells, but Not Monocyte-Derived Dendritic Cells, Can Augment Human NK Cell Function." Cellular Immunology 213, no. 1 (October 2001): 14–23. http://dx.doi.org/10.1006/cimm.2001.1858.

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Rosenzwajg, M., B. Canque, and JC Gluckman. "Human dendritic cell differentiation pathway from CD34+ hematopoietic precursor cells." Blood 87, no. 2 (January 15, 1996): 535–44. http://dx.doi.org/10.1182/blood.v87.2.535.bloodjournal872535.

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The most effective antigen-presenting cells for T lymphocytes are dendritic cells (DCs), the differentiation pathway of which, however, is incompletely characterized. We examined here how DCs differentiated from human cord blood CD34+ progenitor cells cultured with granulocyte- macrophage colony-stimulating factor, tumor necrosis factor-alpha, and stem cell factor. After 5 days, 2 of 3 nonadherent cells were CD13hiHLA- DRhiCD4+, half of them were also CD14+, and < or = 10% were CD1a+. When day-5 sorted CD13hiCD1a- and CD13lo cells were further cultured, CD1a+ cells appeared in the already CD13hi population, whereas CD13hi cells, a minority of which rapidly became CD1a+, emerged from the CD13lo population. By day 12, still 66% of bulk cells in suspension were CD13hi, most of which displayed high forward and side scatters of large granular cells. Half of CD13hi cells were CD1a+. All CD13hi cells expressed to the same extent DR, CD4, costimulatory and adhesion molecules, and various amounts of CD14. CD1a+ cells stimulated allogeneic lymphocytes more than CD13hiCD1a- cells and, although they were CD14+, both cell types were nonspecific esterase-negative nonphagocytic cells and were stronger mixed leukocyte reaction stimulators than were their macrophage counterparts. Eventually, the percentage of CD1a+ cells decreased. However, typical CD1a+ DCs still emerged in culture of sorted day-12 CD13hiCD1a- cells, and adding interleukin-4 to bulk cultures at that time led to the persistence of the CD1a+ population while diminishing CD14 expression. Thus, this system results first in the differentiation of CD13hi precursors that strongly express DR and CD4, from which more mature CD1a+ DCs continuously differentiate all along the culture period.

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Kiama, Stephen Gitahi, Donatus Dreher, Laurence Cochand, Menno Kok, Carolina Obregon, Laurent Nicod, and Peter Gehr. "Host cell responses of Salmonella typhimurium infected human dendritic cells." Immunology & Cell Biology 84, no. 5 (October 2006): 475–81. http://dx.doi.org/10.1111/j.1440-1711.2006.01461.x.

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Kassianos, Andrew J., Sandeep Sampangi, Xiangju Wang, Kathrein E. Roper, Ken Beagley, Helen Healy, and Ray Wilkinson. "Human proximal tubule epithelial cells modulate autologous dendritic cell function." Nephrology Dialysis Transplantation 28, no. 2 (May 18, 2012): 303–12. http://dx.doi.org/10.1093/ndt/gfs136.

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Ishimoto, Hiroshi, Katsunori Yanagihara, Nobuko Araki, Hiroshi Mukae, Noriho Sakamoto, Koichi Izumikawa, Masafumi Seki, et al. "Single-Cell Observation of Phagocytosis by Human Blood Dendritic Cells." Japanese Journal of Infectious Diseases 61, no. 4 (July 28, 2008): 294–97. http://dx.doi.org/10.7883/yoken.jjid.2008.294.

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Yin, Xiangyun, Shuting Chen, and Stephanie C. Eisenbarth. "Dendritic Cell Regulation of T Helper Cells." Annual Review of Immunology 39, no. 1 (April 26, 2021): 759–90. http://dx.doi.org/10.1146/annurev-immunol-101819-025146.

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As the professional antigen-presenting cells of the immune system, dendritic cells (DCs) sense the microenvironment and shape the ensuing adaptive immune response. DCs can induce both immune activation and immune tolerance according to the peripheral cues. Recent work has established that DCs comprise several phenotypically and functionally heterogeneous subsets that differentially regulate T lymphocyte differentiation. This review summarizes both mouse and human DC subset phenotypes, development, diversification, and function. We focus on advances in our understanding of how different DC subsets regulate distinct CD4+ T helper (Th) cell differentiation outcomes, including Th1, Th2, Th17, T follicular helper, and T regulatory cells. We review DC subset intrinsic properties, local tissue microenvironments, and other immune cells that together determine Th cell differentiation during homeostasis and inflammation.

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Langhoff, E., and R. M. Steinman. "Clonal expansion of human T lymphocytes initiated by dendritic cells." Journal of Experimental Medicine 169, no. 1 (January 1, 1989): 315–20. http://dx.doi.org/10.1084/jem.169.1.315.

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The accessory cell requirements for cloning T cells in the presence of lectin and T cell growth factors were examined with cells from human peripheral blood. We found that dendritic cells were active and perhaps essential. Single CD4+ lymphocytes could be cloned with 80% efficiency, and CD8+ cells with 50-60% efficiency if 10(3) syngeneic or allogeneic dendritic cells were added. Some T cell clones developed even with one dendritic cell. Monocytes or B lymphocytes from blood were at least 100-fold weaker in supporting clonal growth. These findings suggest a specialized feeder cell requirement, namely dendritic cells, for cloning T lymphocytes from single resting precursors.

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Bender, A., L. K. Bui, M. A. Feldman, M. Larsson, and N. Bhardwaj. "Inactivated influenza virus, when presented on dendritic cells, elicits human CD8+ cytolytic T cell responses." Journal of Experimental Medicine 182, no. 6 (December 1, 1995): 1663–71. http://dx.doi.org/10.1084/jem.182.6.1663.

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Inactivated or subunit virus preparations have been excellent vaccines for inducing antibody responses. Generation of cytolytic T cell responses, however, is thought to require replicating virus, primarily to provide sufficiently large amounts of cytoplasmic proteins for processing and presentation on major histocompatibility complex class I molecules by antigen-presenting cells. Potent human CD8+ cytolytic T cell responses to live replicating influenza A virus are generated when dendritic cells are used as the antigen-presenting cells. Here, we demonstrate that dendritic cells pulsed with poorly replicating, heat- or ultraviolet-inactivated influenza virus, induce equally strong CD8+ cytolytic T lymphocyte responses. The cytotoxic T lymphocytes are generated in the apparent absence of CD4+ helper cells or exogenous cytokines. Active viral protein synthesis is not required to charge class I molecules on dendritic cells. When pulsed with inactivated virus, < 1% of dendritic cells express nonstructural protein 1, which is only synthesized in the infectious cycle. To be optimally effective, however, the inactivated virus must retain its fusogenic activity, and presumably access the cytoplasm of dendritic cells. The data indicate, therefore, that dendritic cells require only small amounts of viral protein to charge class I molecules, most likely via traditional class I processing pathways. These results reopen the potential use of inactivated virus preparations as immunogens for cytotoxic T lymphocyte responses.

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