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Journal articles on the topic 'Dendritic cells Antigen presentation'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Doe, W., and P. Pavli. "Antigen Presentation in the Gut." Canadian Journal of Gastroenterology 4, no. 7 (1990): 267–70. http://dx.doi.org/10.1155/1990/527602.

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The induction of T cell responses requires recognition of antigens in association with class II major histocompatibility complex (MHC) proteins and specialized antigen-presenting cells. Candidate antigen-presenting cells in the gut include dendritic cells, macrophages, B lymphocytes, mucosal epithelial cells and endothelial cells. Dendritic cells isolated from normal human colon are potent inducers of primary immune responses and express high levels of class lI MHC proteins. Lamina propria macrophages display class II MHC proteins, can present antigens to sensitized T cells, may process antige

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2

Cheminay, Cédric, Annette Möhlenbrink, and Michael Hensel. "IntracellularSalmonellaInhibit Antigen Presentation by Dendritic Cells." Journal of Immunology 174, no. 5 (2005): 2892–99. http://dx.doi.org/10.4049/jimmunol.174.5.2892.

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Petersen, Troels R., Nina Dickgreber, and Ian F. Hermans. "Tumor Antigen Presentation by Dendritic Cells." Critical Reviews™ in Immunology 30, no. 4 (2010): 345–86. http://dx.doi.org/10.1615/critrevimmunol.v30.i4.30.

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4

Sunshine, Geoffrey H., and Tamara J. Mitchell. "Antigen Presentation by Spleen Dendritic Cells." Journal of Investigative Dermatology 85, no. 1 (1985): S110—S114. http://dx.doi.org/10.1111/1523-1747.ep12275577.

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5

Chung, Yeonseok, Jae-Hoon Chang, Mi-Na Kweon, Paul D. Rennert та Chang-Yuil Kang. "CD8α–11b+ dendritic cells but not CD8α+ dendritic cells mediate cross-tolerance toward intestinal antigens". Blood 106, № 1 (2005): 201–6. http://dx.doi.org/10.1182/blood-2004-11-4240.

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Cross-presentation is a critical process by which antigen is displayed to CD8 T cells to induce tolerance. It is believed that CD8α+ dendritic cells (DCs) are responsible for cross-presentation, suggesting that the CD8α+ DC population is capable of inducing both cross-priming and cross-tolerance to antigen. We found that cross-tolerance against intestinal soluble antigen was abrogated in C57BL/6 mice lacking mesenteric lymph nodes (MLNs) and Peyer patches (PPs), whereas mice lacking PPs alone were capable of developing CD8 T-cell tolerance. CD8α–CD11b+ DCs but not CD8α+ DCs in the MLNs present

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6

McCloskey, Megan L., Maria A. Curotto de Lafaille, Michael C. Carroll, and Adrian Erlebacher. "Acquisition and presentation of follicular dendritic cell–bound antigen by lymph node–resident dendritic cells." Journal of Experimental Medicine 208, no. 1 (2010): 135–48. http://dx.doi.org/10.1084/jem.20100354.

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Follicular dendritic cells (DCs [FDCs]) are prominent stromal cell constituents of B cell follicles with the remarkable ability to retain complement-fixed antigens on their cell surface for extended periods of time. These retained immune complexes have long been known to provide the antigenic stimulus that drives antibody affinity maturation, but their role in cellular immunity has remained unclear. In this study, we show that FDC-retained antigens are continually sampled by lymph node–resident DCs for presentation to CD8 T cells. This novel pathway of antigen acquisition was detectable when F

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Sallusto, Federica, Chiara Nicolò, Ruggero De Maria, Silvia Corinti, and Roberto Testi. "Ceramide Inhibits Antigen Uptake and Presentation by Dendritic Cells." Journal of Experimental Medicine 184, no. 6 (1996): 2411–16. http://dx.doi.org/10.1084/jem.184.6.2411.

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Ceramides are intramembrane diffusible mediators involved in transducing signals originated from a variety of cell surface receptors. Different adaptive and differentiative cellular responses, including apoptotic cell death, use ceramide-mediated pathways as an essential part of the program. Here, we show that human dendritic cells respond to CD40 ligand, as well as to tumor necrosis factor-α and IL-1β, with intracellular ceramide accumulation, as they are induced to differentiate. Dendritic cells down-modulate their capacity to take up soluble antigens in response to exogenously added or endo

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8

Nierkens, Stefan, and Edith M. Janssen. "Harnessing Dendritic Cells for Tumor Antigen Presentation." Cancers 3, no. 2 (2011): 2195–213. http://dx.doi.org/10.3390/cancers3022195.

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9

Inaba, Kayo, and Muneo Inaba. "Antigen Recognition and Presentation by Dendritic Cells." International Journal of Hematology 81, no. 3 (2005): 181–87. http://dx.doi.org/10.1532/ijh97.04200.

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10

Eken, Ahmet, Vivian Ortiz, and Jack R. Wands. "Ethanol Inhibits Antigen Presentation by Dendritic Cells." Clinical and Vaccine Immunology 18, no. 7 (2011): 1157–66. http://dx.doi.org/10.1128/cvi.05029-11.

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ABSTRACTPrevious studies suggest that altered virus-specific T-cell responses observed during chronic ethanol exposure may be due to abnormal functioning of dendritic cells (DCs). Here we explored the effects of ethanol on exogenous antigen presentation by DCs. BALB/c, C57BL/6, and CBA/caj mice were fed ethanol or an isocaloric control diet for 8 weeks. The splenic DC population was expanded using an Flt3L expression plasmid via tail vein injection. DCs were purified and assessed for antigen presentation and processing and for peptide-major histocompatibility complex class I and II (MHCI and M

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11

Mougneau, Evelyne, Stéphanie Hugues, and Nicolas Glaichenhaus. "Antigen Presentation by Dendritic Cells In Vivo." Journal of Experimental Medicine 196, no. 8 (2002): 1013–16. http://dx.doi.org/10.1084/jem.20021636.

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12

Savina, Ariel, and Sebastian Amigorena. "Phagocytosis and antigen presentation in dendritic cells." Immunological Reviews 219, no. 1 (2007): 143–56. http://dx.doi.org/10.1111/j.1600-065x.2007.00552.x.

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13

Segura, Elodie, and José A. Villadangos. "Antigen presentation by dendritic cells in vivo." Current Opinion in Immunology 21, no. 1 (2009): 105–10. http://dx.doi.org/10.1016/j.coi.2009.03.011.

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14

Villadangos, José A., and Louise Young. "Antigen-Presentation Properties of Plasmacytoid Dendritic Cells." Immunity 29, no. 3 (2008): 352–61. http://dx.doi.org/10.1016/j.immuni.2008.09.002.

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15

Brinker, Karen G., Emily Martin, Paul Borron, et al. "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 (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

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16

Benitez-Ribas, Daniel, Gosse J. Adema, Gregor Winkels та ін. "Plasmacytoid dendritic cells of melanoma patients present exogenous proteins to CD4+ T cells after FcγRII-mediated uptake". Journal of Experimental Medicine 203, № 7 (2006): 1629–35. http://dx.doi.org/10.1084/jem.20052364.

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Plasmacytoid dendritic cells (pDCs) contribute to innate antiviral immune responses by producing type I interferons. Although human pDCs can induce T cell responses upon viral infection, it remains unclear if pDCs can present exogenous antigens. Here, we show that human pDCs exploit FcγRII (CD32) to internalize antigen–antibody complexes, resulting in the presentation of exogenous antigen to T cells. pDCs isolated from melanoma patients vaccinated with autologous monocyte-derived peptide- and keyhold limpet hemocyanin (KLH)–loaded dendritic cells, but not from nonvaccinated patients or patient

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17

Fu, Chunmei, Peng Peng, Jakob Loschko, et al. "Plasmacytoid dendritic cells cross-prime naive CD8 T cells by transferring antigen to conventional dendritic cells through exosomes." Proceedings of the National Academy of Sciences 117, no. 38 (2020): 23730–41. http://dx.doi.org/10.1073/pnas.2002345117.

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Although plasmacytoid dendritic cells (pDCs) have been shown to play a critical role in generating viral immunity and promoting tolerance to suppress antitumor immunity, whether and how pDCs cross-prime CD8 T cells in vivo remain controversial. Using a pDC-targeted vaccine model to deliver antigens specifically to pDCs, we have demonstrated that pDC-targeted vaccination led to strong cross-priming and durable CD8 T cell immunity. Surprisingly, cross-presenting pDCs required conventional DCs (cDCs) to achieve cross-priming in vivo by transferring antigens to cDCs. Taking advantage of an in vitr

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18

Rodriguez-Fernandez, Jose Luis. "Antigen Presentation by Dendritic Cells in Rheumatoid Arthritis." Current Topics in Medicinal Chemistry 13, no. 6 (2013): 712–19. http://dx.doi.org/10.2174/1568026611313060004.

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19

Watts, Colin, Michele A. West, and Rossana Zaru. "TLR signalling regulated antigen presentation in dendritic cells." Current Opinion in Immunology 22, no. 1 (2010): 124–30. http://dx.doi.org/10.1016/j.coi.2009.12.005.

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20

Inaba, K., J. P. Metlay, M. T. Crowley, and R. M. Steinman. "Dendritic cells pulsed with protein antigens in vitro can prime antigen-specific, MHC-restricted T cells in situ." Journal of Experimental Medicine 172, no. 2 (1990): 631–40. http://dx.doi.org/10.1084/jem.172.2.631.

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T cells recognize peptides that are bound to MHC molecules on the surface of different types of antigen-presenting cells (APC). Antigen presentation most often is studied using T cells that have undergone priming in situ, or cell lines that have been chronically stimulated in vitro. The use of primed cells provides sufficient numbers of antigen-reactive lymphocytes for experimental study. A more complete understanding of immunogenicity, however, requires that one develop systems for studying the onset of a T cell response from unprimed lymphocytes, especially in situ. Here it is shown that mou

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21

Ayinde, Diana, Timothée Bruel, Sylvain Cardinaud, et al. "SAMHD1 Limits HIV-1 Antigen Presentation by Monocyte-Derived Dendritic Cells." Journal of Virology 89, no. 14 (2015): 6994–7006. http://dx.doi.org/10.1128/jvi.00069-15.

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ABSTRACTMonocyte-derived dendritic cells (MDDC) stimulate CD8+cytotoxic T lymphocytes (CTL) by presenting endogenous and exogenous viral peptides via major histocompatibility complex class I (MHC-I) molecules. MDDC are poorly susceptible to HIV-1, in part due to the presence of SAMHD1, a cellular enzyme that depletes intracellular deoxynucleoside triphosphates (dNTPs) and degrades viral RNA. Vpx, an HIV-2/SIVsm protein absent from HIV-1, antagonizes SAMHD1 by inducing its degradation. The impact of SAMHD1 on the adaptive cellular immune response remains poorly characterized. Here, we asked whe

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22

Cheadle, Eleanor J., Dearbhaile O'Donnell, Peter J. Selby, and Andrew M. Jackson. "Closely Related Mycobacterial Strains Demonstrate Contrasting Levels of Efficacy as Antitumor Vaccines and Are Processed for Major Histocompatibility Complex Class I Presentation by Multiple Routes in Dendritic Cells." Infection and Immunity 73, no. 2 (2005): 784–94. http://dx.doi.org/10.1128/iai.73.2.784-794.2005.

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ABSTRACT Mycobacteria expressing recombinant antigens are already being developed as vaccines against both infections and tumors. Little is known about how dendritic cells might process such antigens. Two different mycobacterial species, the fast-growing Mycobacterium smegmatis and the slow-growing M. bovis M. bovis BCG, were engineered to express a model tumor antigen, the Kb-restricted dominant cytotoxic T-lymphocyte epitope OVA257-264. Recombinant M. bovis BCG but not recombinant M. smegmatis conferred protection to mice challenged with the B16-OVA tumor cell line. We went on to investigate

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23

Wang, Xiaojian, Hongmei Li, Catherine Matte-Martone, et al. "Mechanisms of antigen presentation to T cells in murine graft-versus-host disease: cross-presentation and the appearance of cross-presentation." Blood 118, no. 24 (2011): 6426–37. http://dx.doi.org/10.1182/blood-2011-06-358747.

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Abstract Recipient antigen-presenting cells (APCs) initiate GVHD by directly presenting host minor histocompatibility antigens (miHAs) to donor CD8 cells. However, later after transplantation, host APCs are replaced by donor APCs, and if pathogenic CD8 cells continue to require APC stimulation, then donor APCs must cross-present host miHAs. Consistent with this, CD8-mediated GVHD is reduced when donor APCs are MHC class I−. To study cross-presentation, we used hosts that express defined MHC class I Kb-restricted miHAs, crossed to Kb-deficient backgrounds, such that these antigens cannot be dir

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24

Liu, L. M., and G. G. MacPherson. "Antigen acquisition by dendritic cells: intestinal dendritic cells acquire antigen administered orally and can prime naive T cells in vivo." Journal of Experimental Medicine 177, no. 5 (1993): 1299–307. http://dx.doi.org/10.1084/jem.177.5.1299.

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In the rat, mesenteric lymphadenectomy allows collection of dendritic cells (DC) derived from the small intestine after cannulation of the thoracic duct. We prepared rats this way and administered antigens by oral feeding or intraintestinal injection. DC enriched from the thoracic duct lymph collected over the first 24 h from these animals are able to stimulate sensitized T cells in vitro and to prime popliteal lymph node CD4+ T cells after footpad injection, while B and T cells from the same thoracic duct lymph are inert in priming. 500 or less DC pulsed in vitro with antigen can prime T cell

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25

Klechevsky, Eynav, Anne-Laure Flamar, Yanying Cao, et al. "Cross-priming CD8+ T cells by targeting antigens to human dendritic cells through DCIR." Blood 116, no. 10 (2010): 1685–97. http://dx.doi.org/10.1182/blood-2010-01-264960.

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Abstract We evaluated human CD8+ T-cell responses generated by targeting antigens to dendritic cells (DCs) through various lectin receptors. We found the immunoreceptor tyrosine-based inhibitory motif-containing DC immunoreceptor (DCIR) to mediate potent cross-presentation. A single exposure to a low dose of anti-DCIR–antigen conjugate initiated antigen-specific CD8+ T-cell immunity by all human DC subsets including ex vivo–generated DCs, skin-isolated Langerhans cells, and blood myeloid DCs and plasmacytoid DCs. The delivery of influenza matrix protein (FluMP) through DCIR resulted in expansi

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26

Kowalczyk, Dariusz W. "Tumors and the danger model." Acta Biochimica Polonica 49, no. 2 (2002): 295–302. http://dx.doi.org/10.18388/abp.2002_3787.

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This article reviews the evidence for the danger model in the context of immune response to tumors and the insufficiency of the immune system to eliminate tumor growth. Despite their potential immunogenicity tumors do not induce significant immune responses which could destroy malignant cells. According to the danger model, the immune surveillance system fails to detect tumor antigens because transformed cells do not send any danger signals which could activate dendritic cells and initiate an immune response. Instead, tumor cells or antigen presenting cells turn off the responding T cells and

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27

Graham, Daniel B., Linda M. Stephenson, Siu Kit Lam, et al. "An ITAM-signaling pathway controls cross-presentation of particulate but not soluble antigens in dendritic cells." Journal of Experimental Medicine 204, no. 12 (2007): 2889–97. http://dx.doi.org/10.1084/jem.20071283.

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Dendritic cells (DC) possess a unique capacity for presenting exogenous antigen on major histocompatibility class I, a process that is referred to as cross-presentation, which serves a critical role in microbial and tumor immunity. During cross-presentation, antigens derived from pathogen-infected or tumor cells are internalized and processed by DCs for presentation to cytotoxic T lymphocytes (CTLs). We demonstrate that a signaling pathway initiated by the immunoreceptor tyrosine–based activation motif (ITAM)–containing adaptors DAP12 and FcRγ utilizes the Vav family of Rho guanine nucleotide

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28

Moris, Arnaud, Anthony Pajot, Fabien Blanchet, Florence Guivel-Benhassine, Margarita Salcedo, and Olivier Schwartz. "Dendritic cells and HIV-specific CD4+ T cells: HIV antigen presentation, T-cell activation, and viral transfer." Blood 108, no. 5 (2006): 1643–51. http://dx.doi.org/10.1182/blood-2006-02-006361.

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Human immunodeficiency virus (HIV)-specific CD4+ lymphocytes are preferentially infected in HIV-positive individuals. To study this preferential infection, we have derived several HIV-specific (HS) CD4+ clones. We show that in dendritic cells (DCs), HIV virion capture led to major histocompatibility complex class-II (MHC-II)-restricted viral antigen presentation and to activation of HS cells. In contrast, neither cell-free virions nor infected lymphocytes activated HS cells. In DCs, the dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN/CD209), which intern

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29

Shurin, Galina V., Irina L. Tourkova, Gurkamal S. Chatta, et al. "Small Rho GTPases Regulate Antigen Presentation in Dendritic Cells." Journal of Immunology 174, no. 6 (2005): 3394–400. http://dx.doi.org/10.4049/jimmunol.174.6.3394.

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30

McBride, W. H., Y. Liao, L. Butterfield, and A. Ribas. "Ionizing radiation affects tumor antigen presentation by dendritic cells." International Journal of Radiation Oncology*Biology*Physics 57, no. 2 (2003): S258. http://dx.doi.org/10.1016/s0360-3016(03)01096-4.

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31

Smith, Christopher M., Michael B. Gill, Janet S. May, and Philip G. Stevenson. "Murine Gammaherpesvirus-68 Inhibits Antigen Presentation by Dendritic Cells." PLoS ONE 2, no. 10 (2007): e1048. http://dx.doi.org/10.1371/journal.pone.0001048.

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32

Théry, Clotilde, and Sebastian Amigorena. "The cell biology of antigen presentation in dendritic cells." Current Opinion in Immunology 13, no. 1 (2001): 45–51. http://dx.doi.org/10.1016/s0952-7915(00)00180-1.

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33

Chen, Guoyou, Lin Lu, Yingming Jiang, Yi Zhang, and Xuetao Cao. "Interleukin-24 Promotes Dendritic Cells Maturation and Antigen Presentation." Journal of Immunotherapy 27, no. 6 (2004): S13—S14. http://dx.doi.org/10.1097/00002371-200411000-00053.

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34

Hoffmann, E., F. Kotsias, G. Visentin, P. Bruhns, A. Savina, and S. Amigorena. "Autonomous phagosomal degradation and antigen presentation in dendritic cells." Proceedings of the National Academy of Sciences 109, no. 36 (2012): 14556–61. http://dx.doi.org/10.1073/pnas.1203912109.

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35

Santambrogio, L., A. K. Sato, G. J. Carven, S. L. Belyanskaya, J. L. Strominger, and L. J. Stern. "Extracellular antigen processing and presentation by immature dendritic cells." Proceedings of the National Academy of Sciences 96, no. 26 (1999): 15056–61. http://dx.doi.org/10.1073/pnas.96.26.15056.

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36

Mizumoto, Norikatsu, Hiroaki Tanaka, Hironori Matsushima, Mridula Vishwanath, and Akira Takashima. "Colchicine Promotes Antigen Cross-Presentation by Murine Dendritic Cells." Journal of Investigative Dermatology 127, no. 6 (2007): 1543–46. http://dx.doi.org/10.1038/sj.jid.5700699.

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37

Amigorena, Sebastian, and Ariel Savina. "Intracellular mechanisms of antigen cross presentation in dendritic cells." Current Opinion in Immunology 22, no. 1 (2010): 109–17. http://dx.doi.org/10.1016/j.coi.2010.01.022.

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38

Heath, William R., Yu Kato, Thiago M. Steiner, and Irina Caminschi. "Antigen presentation by dendritic cells for B cell activation." Current Opinion in Immunology 58 (June 2019): 44–52. http://dx.doi.org/10.1016/j.coi.2019.04.003.

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39

Dresch, Christiane, Yann Leverrier, Jacqueline Marvel, and Ken Shortman. "Development of antigen cross-presentation capacity in dendritic cells." Trends in Immunology 33, no. 8 (2012): 381–88. http://dx.doi.org/10.1016/j.it.2012.04.009.

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40

Breman, Eytan, Jurjen M. Ruben, Kees L. Franken, et al. "Uptake of HLA Alloantigens via CD89 and CD206 Does Not Enhance Antigen Presentation by Indirect Allorecognition." Journal of Immunology Research 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/4215684.

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In organ transplantation, alloantigens are taken up by antigen presenting cells and presented via the indirect pathway to T-cells which in turn can induce allograft rejection. Monitoring of these T-cells is of major importance; however no reliable assay is available to routinely monitor indirect allorecognition. Recently we showed that HLA monomers can be successfully used to monitor indirect allorecognition. Targeting antigens to endocytic receptors on antigen presenting cells may further enhance the presentation of antigens via HLA class II and improve the efficiency of this assay. In the cu

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41

Inaba, K., M. Inaba, M. Naito, and R. M. Steinman. "Dendritic cell progenitors phagocytose particulates, including bacillus Calmette-Guerin organisms, and sensitize mice to mycobacterial antigens in vivo." Journal of Experimental Medicine 178, no. 2 (1993): 479–88. http://dx.doi.org/10.1084/jem.178.2.479.

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Dendritic cells, while effective in sensitizing T cells to several different antigens, show little or no phagocytic activity. To the extent that endocytosis is required for antigen processing and presentation, it is not evident how dendritic cells would present particle-associated peptides. Evidence has now been obtained showing that progenitors to dendritic cells can internalize particles, including Bacillus Calmette-Guerin (BCG) mycobacteria. The particulates are applied for 20 h to bone marrow cultures that have been stimulated with granulocyte/macrophage colony-stimulating factor (GM-CSF)

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Garrigan, K., P. Moroni-Rawson, C. McMurray, et al. "Functional comparison of spleen dendritic cells and dendritic cells cultured in vitro from bone marrow precursors." Blood 88, no. 9 (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

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Kaneko, T., T. Okiji, R. Kaneko, J. E. Nör, and H. Suda. "Antigen-presenting Cells in Human Radicular Granulomas." Journal of Dental Research 87, no. 6 (2008): 553–57. http://dx.doi.org/10.1177/154405910808700617.

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Substantial numbers of dendritic cells have been detected in radicular granulomas. To test the hypothesis that local antigen presentation from dendritic cells to T-cells is involved critically in immunological responses within radicular granulomas, we compared characteristics of dendritic cells and macrophages by morphological and biological analyses. Under light microscopy, HLA-DR+ and CD68+ cells showed diverse profiles, including dendritic-shaped cells. Transmission electron microscopy revealed that HLA-DR+ dendritic cells, with long cytoplasmic processes and lacking distinct phagosomes, we

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44

Matheoud, Diana, Leila Perié, Guillaume Hoeffel, et al. "Cross-presentation by dendritic cells from live cells induces protective immune responses in vivo." Blood 115, no. 22 (2010): 4412–20. http://dx.doi.org/10.1182/blood-2009-11-255935.

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Abstract Cross-presentation is an essential mechanism that allows dendritic cells (DCs) to efficiently present exogenous antigens to CD8+ T cells. Among cellular antigen sources, apoptotic cells are commonly considered as the best for cross-presentation by DCs. However, the potential of live cells as a source of antigen has been overlooked. Here we explored whether DCs were able to capture and cross-present antigens from live cells. DCs internalized cytosolic and membrane material into vesicles from metabolically labeled live cells. Using time-lapse confocal microscopy in whole spleens, we sho

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Honda, Tetsuya, Gyohei Egawa, and Kenji Kabashima. "Antigen presentation and adaptive immune responses in skin." International Immunology 31, no. 7 (2019): 423–29. http://dx.doi.org/10.1093/intimm/dxz005.

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Abstract For the induction of adequate cutaneous immune responses, the antigen presentation and recognition that occur in both the skin and skin-draining lymph nodes are essential. In each process of cutaneous immune responses, several distinct subsets of immune cells, including dendritic cells and T cells, are involved, and they elicit their respective functions in a harmonious manner. For example, in the elicitation phase of cutaneous acquired immunity, immune cells form a specific lymphoid structure named inducible skin-associated lymphoid tissue (iSALT) to facilitate efficient antigen pres

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46

Bruña-Romero, Oscar, and Ana Rodriguez. "Dendritic Cells Can Initiate Protective Immune Responses against Malaria." Infection and Immunity 69, no. 8 (2001): 5173–76. http://dx.doi.org/10.1128/iai.69.8.5173-5176.2001.

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ABSTRACT An understanding of the antigen presentation mechanisms that mediate induction of protective immune responses against malaria is essential for the development of successful immunization approaches. Here we show that dendritic cells presenting Plasmodium yoelii sporozoite antigens are able to activate specific CD4+ and CD8+ T cells and initiate protective immune responses against malaria in mice.

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47

Blachère, Nathalie E., Robert B. Darnell, and Matthew L. Albert. "Apoptotic Cells Deliver Processed Antigen to Dendritic Cells for Cross-Presentation." PLoS Biology 3, no. 6 (2005): e185. http://dx.doi.org/10.1371/journal.pbio.0030185.

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48

Cohn, Lillian, Bithi Chatterjee, Filipp Esselborn, et al. "Antigen delivery to early endosomes eliminates the superiority of human blood BDCA3+ dendritic cells at cross presentation." Journal of Experimental Medicine 210, no. 5 (2013): 1049–63. http://dx.doi.org/10.1084/jem.20121251.

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Human BDCA3+ dendritic cells (DCs), the proposed equivalent to mouse CD8α+ DCs, are widely thought to cross present antigens on MHC class I (MHCI) molecules more efficiently than other DC populations. If true, it is unclear whether this reflects specialization for cross presentation or a generally enhanced ability to present antigens on MHCI. We compared presentation by BDCA3+ DCs with BDCA1+ DCs using a quantitative approach whereby antigens were targeted to distinct intracellular compartments by receptor-mediated internalization. As expected, BDCA3+ DCs were superior at cross presentation of

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Kavanagh, Daniel G., Daniel E. Kaufmann, Sherzana Sunderji, et al. "Expansion of HIV-specific CD4+ and CD8+ T cells by dendritic cells transfected with mRNA encoding cytoplasm- or lysosome-targeted Nef." Blood 107, no. 5 (2006): 1963–69. http://dx.doi.org/10.1182/blood-2005-04-1513.

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Transfection with synthetic mRNA is a safe and efficient method of delivering antigens to dendritic cells for immunotherapy. Targeting antigens to the lysosome can sometimes enhance the CD4+ T-cell response. We transfected antigen-presenting cells (APCs) with mRNA encoding Gag-p24 and cytoplasmic, lysosomal, and secreted forms of Nef. Antigen-specific cytotoxic T cells were able to lyse the majority of transfected targets, indicating that transfection was efficient. Transfection of APCs with a Nef construct bearing lysosomal targeting signals produced rapid and prolonged antigen presentation t

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Szpakowski, Piotr, Dominika Ksiazek-Winiarek, and Andrzej Glabinski. "Targeting Antigen-Presenting Cells in Multiple Sclerosis Treatment." Applied Sciences 11, no. 18 (2021): 8557. http://dx.doi.org/10.3390/app11188557.

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Multiple sclerosis (MS) is common neurological disease of the central nervous system (CNS) affecting mostly young adults. Despite decades of studies, its etiology and pathogenesis are not fully unraveled and treatment is still insufficient. The vast majority of studies suggest that the immune system plays a major role in MS development. This is also supported by the effectiveness of currently available MS treatments that target immunocompetent cells. In this review, the role of antigen-presenting cells (APC) in MS development as well as the novel therapeutic options targeting those cells in MS

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