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Journal articles on the topic 'DCS'

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Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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1

Mazzoccoli, Luciano, Stephen Iwanowycz, Chelsea Peterson, Soo Ngoi, Megan Hill, and Bei Liu. "Molecular chaperone GP96 is a potential target to modulate dendritic cell programming and shape anti-tumor immunity." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 102.28. http://dx.doi.org/10.4049/jimmunol.208.supp.102.28.

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Abstract Dendritic cells (DCs) are professional antigen-presenting cells providing costimulatory signals to adaptive immune cells. Currently, the lack of strategies to improve antigen presentation is a hindrance in tumor immunology. Despite studies focusing on antigen cross-presenting Type-1 DCs (DC1s), a study published by our lab revealed Type-2 DCs (DC2s) with significant survival across multiple human cancers. Our research group has a long-term interest in studying immune chaperone GP96, which is an essential molecular chaperone for TLRs, GARP, and other vital innate receptors. The immune-related client network of GP96 creates opportunities to unmask the roles of multiple receptors on DCs. We have generated DC-specific GP96 deficient mice and reported increased tumor-infiltrating DC2 and delayed tumor development on the spontaneous breast cancer model. However, the mechanism by which GP96 regulates DCs function is under investigation. Using different tumor models, we found that deletion of GP96 on DCs improved immune response and decreased tumor growth. However, macrophage-GP96KO mice showed a loss of benefits observed on DC-GP96KO mice. Also, differential stimulatory/inhibitory molecules on DC1 vs. DC2 were tumor-dependent. To determine the role of DC-intrinsic GP96 in T cell activation, we used in vitro antigen-cross presentation assay. We found that OT-I CD8+ T cell activation was delayed at the initial days of the co-culture with GP96KO DCs but restored in the late phase compared with WT DCs. Collectively, the results show beneficial inflammatory DC2 molecular activation, with DC1 able to cross-present antigens to CD8+ T cells. Our study indicated that targeting GP96 on DCs may contribute to shaping T cell anti-tumor immunity. Supported by grants from NIH NCI (R01:CA193939) and NIH NIAID (U01:AI125859)

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2

Cook, Donald N., Gentaro Izumi, Peer WF Karmaus, and Hideki Nakano. "A novel lung DC(3) population potently induces Th17 responses to inhaled allergens." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 234.1. http://dx.doi.org/10.4049/jimmunol.204.supp.234.1.

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Abstract Allergic asthma is an inflammatory disease of the airways associated with T helper (Th)2-driven eosinophilia and Th17-directed neutrophilia. Although eosinophilic asthma generally responds well to inhaled glucocorticoids, neutrophilic asthma does not, and new therapies are needed for this disease subtype. A consensus DC subset in the lung that strongly promotes Th17 responses to inhaled allergens has remained elusive, as some groups have reported that CD103+ DCs (DC1) promote Th17 differentiation, whereas other groups have attributed this function to CD11bhi DCs (DC2). We hypothesized that this apparent discrepancy might be due to the heterogeneity of lung CD11b+ DCs and therefore used mass cytometry (CyTOF) to study these cells following allergic sensitization through the airway. We identified a novel CD11b+ APC that was recruited to the inflamed airways of mice following their inhalation of house dust extracts. These cells were bona fide DCs, as they were FLT3L-dependent, expressed Zbtb46, and formed dendrites. Bulk RNA-seq analysis of these DCs revealed that their transcriptome was similar to, yet distinct from, that of conventional DC2s. Although the novel DCs promoted only weak Th2 differentiation, they drove robust Th17 differentiation. Single cell RNA-sequencing of total lung CD11bhi DCs revealed seven distinct clusters, two of which co-expressed both Tgfb1 and Il1b. Pseudotime analysis suggested a progression from an immature form of these cells to a more mature form. Together, these findings identify a novel DC population (DC3) in the lung that potently stimulates Th17 responses to inhaled allergens.

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3

Brassard, Julyanne, Meredith Elizabeth Gill, Emilie Bernatchez, Véronique Desjardins, Joanny Roy, Philippe Joubert, David Marsolais, and Marie-Renée Blanchet. "Countering the advert effects of lung cancer on the anticancer potential of dendritic cell populations reinstates sensitivity to anti-PD-1 therapy." PLOS ONE 16, no. 11 (November 30, 2021): e0260636. http://dx.doi.org/10.1371/journal.pone.0260636.

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Lung cancer is the leading cause of cancer-related deaths. While the recent use of immune checkpoint inhibitors significantly improves patient outcomes, responsiveness remains restricted to a small proportion of patients. Conventional dendritic cells (DCs) play a major role in anticancer immunity. In mice, two subpopulations of DCs are found in the lung: DC2s (CD11b+Sirpα+) and DC1s (CD103+XCR1+), the latest specializing in the promotion of anticancer immune responses. However, the impact of lung cancer on DC populations and the consequent influence on the anticancer immune response remain poorly understood. To address this, DC populations were studied in murine models of Lewis Lung Carcinoma (LLC) and melanoma-induced lung metastasis (B16F10). We report that direct exposure to live or dead cancer cells impacts the capacity of DCs to differentiate into CD103+ DC1s, leading to profound alterations in CD103+ DC1 proportions in the lung. In addition, we observed the accumulation of CD103loCD11b+ DCs, which express DC2 markers IRF4 and Sirpα, high levels of T-cell inhibitory molecules PD-L1/2 and the regulatory molecule CD200. Finally, DC1s were injected in combination with an immune checkpoint inhibitor (anti-PD-1) in the B16F10 model of resistance to the anti-PD-1 immune checkpoint therapy; the co-injection restored sensitivity to immunotherapy. Thus, we demonstrate that lung tumor development leads to the accumulation of CD103loCD11b+ DCs with a regulatory potential combined with a reduced proportion of highly-specialized antitumor CD103+ DC1s, which could promote cancer growth. Additionally, promoting an anticancer DC signature could be an interesting therapeutic avenue to increase the efficacy of existing immune checkpoint inhibitors.

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4

Gargaro, Marco, Giulia Scalisi, Carlos G. Briseño, Giorgia Manni, Vivek Durai, Prachi Bagadia, Paolo Puccetti, Theresa L. Murphy, Kenneth M. Murphy, and Francesca Fallarino. "A novel kynurenine-dependent circuit in DC1 promote IDO1 expression in DC2 leading to experimental autoimmune encephalomyelitis suppression." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 46.19. http://dx.doi.org/10.4049/jimmunol.200.supp.46.19.

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Abstract Classical dendritic cells (cDCs) are professional antigen-presenting cells that play a key role in shaping appropriate immune responses. DCs are a potent T cell activators but they are also involved in maintaining immune homeostasis and self-tolerance. DCs can be classified into three major types: pDC, DC1 and DC2. One mechanism by which DCs regulate tolerance involves indoleamine 2,3-dioxygenase 1 (IDO1) a tryptophan (Trp) metabolizing enzyme. In this study, we analyzed the ability of L-Kyn to induce tolerogenic IDO1 pathway in different DCs subsets in vitro and in vivo model of experimental autoimmune encephalomyelitis (EAE). We show that inflammatory stimuli, like LPS, was able to induce IDO1 only in DC1, but not in DC2 or pDC, when DCs were treated as isolated cultures. In contrast, when LPS was added to cultures containing all three DC subsets, LPS could also induce IDO1 expression in DC2, which acquired tolerogenic function. Induction of IDO1 in DC2 involved a novel DC1-DC2 communication pathway mediated by a Kyn-AhR-RelB axis. Kynurenine produced by DC1 activates AhR in DC2 inducing IDO1 in a RelB-dependent manner. In vitro L-Kyn treatment impaired DC2 T cells priming ability causing suppression of MOG-specific reactivity with an increment of Foxp3+ CD4+ T cells. In vivo, oral administration of L-Kyn induces functional Treg cells that suppress EAE and this effect is completely abrogated in Ahrflox/floxCD11C Cre+ mice. These data suggest that in specific microenvironments, small numbers of IDO1-expressing DC1 may spread tolerogenic activity to DC2 cells through a kynurenine-AhR axis and L-Kyn could constituting a unique endogenous molecule for therapeutic immunomodulation of inflammatory and autoimmune diseases.

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5

Craig, A. "DCS 15." Journal of The Royal Naval Medical Service 80, no. 3 (1994): 116–17. http://dx.doi.org/10.1136/jrnms-80-116.

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6

Cuevas, Ángel, Manuel Urueña, Gustavo de Veciana, and Aditya Yadav. "STARR-DCS." ACM Transactions on Sensor Networks 10, no. 1 (November 2013): 1–37. http://dx.doi.org/10.1145/2529980.

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7

Fehervari, Zoltan. "DCs remember." Nature Immunology 20, no. 9 (August 20, 2019): 1089. http://dx.doi.org/10.1038/s41590-019-0486-y.

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8

Dempsey, Laurie A. "Regulatory DCs." Nature Immunology 21, no. 5 (April 23, 2020): 488. http://dx.doi.org/10.1038/s41590-020-0683-8.

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9

Fehervari, Zoltan. "Decrepit DCs." Nature Immunology 15, no. 11 (October 20, 2014): 1008. http://dx.doi.org/10.1038/ni.3021.

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10

Ngoi, Soo, Yi Yang, Stephen Iwanowycz, Jennifer Gutierrez, Yingqi Li, Christina Williams, Megan Hill, Dongjun Chung, Carter Allen, and Bei Liu. "Migrating Type 2 Dendritic Cells Prime Mucosal Th17 Cells Specific to Small Intestinal Commensal Bacteria." Journal of Immunology 209, no. 6 (September 15, 2022): 1200–1211. http://dx.doi.org/10.4049/jimmunol.2200204.

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Abstract Dendritic cells (DCs) are professional APCs equipped with MHC-restricted Ags, costimulations, and cytokines that effectively prime and differentiate naive T cells into distinct functional subsets. The immune signals that DCs carry reflect the route of Ag uptake and the innate stimuli they received. In the mucosal tissues, owing to the great variety of foreign Ags and inflammatory cues, DCs are predominantly activated and migratory. In the small intestine, CD4 Th17 cells are abundant and have been shown to be regulated by DCs and macrophages. Using a mouse commensal bacteria experimental model, we identified that the early priming step of commensal-driven Th17 cells is controlled by bona fide Zbtb46-expressing DCs. CCR7-dependent migration of type 2 DCs (DC2s) from the small intestine to the mesenteric lymph nodes (MLNs) is essential for the activation of naive CD4 T cells. The migratory DC2 population in the MLNs is almost exclusively Esam+ cells. Single-cell RNA sequencing highlighted the abundance of costimulatory markers (CD40 and OX40) and chemokines (Ccl22 and Cxcl16) on MLN migratory DCs. Further resolution of MLN migratory DC2s revealed that the Th17-polarizing cytokine IL-6 colocalizes with DC2s expressing CD40, Ccl17, and Ccl22. Thus, early Th17 cell differentiation is initiated by a small subset of migratory DC2s in the gut-draining lymph nodes.

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11

O'Keeffe, Meredith, Hubertus Hochrein, David Vremec, Bernadette Scott, Paul Hertzog, Lilliana Tatarczuch, and Ken Shortman. "Dendritic cell precursor populations of mouse blood: identification of the murine homologues of human blood plasmacytoid pre-DC2 and CD11c+ DC1 precursors." Blood 101, no. 4 (February 15, 2003): 1453–59. http://dx.doi.org/10.1182/blood-2002-03-0974.

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Immature and predendritic cells (pre-DCs) of human blood are the most readily accessible human DC sources available for study ex vivo. Murine homologues of human blood DCs have not been described. We report the isolation and characterization of 2 populations of precursor DCs in mouse blood. Mouse blood cells with the surface phenotype CD11cloCD11b−CD45RAhi closely resemble human plasmacytoid cells (or pre-DC2) by morphology and function. On stimulation with oligonucleotides containing CpG motifs (CpG), these cells make large amounts of type 1 interferons and rapidly develop into DCs that bear CD8, though they may be distinct from the CD8+ DCs in the unstimulated mouse. A second population of cells with the surface phenotype CD11c+CD11b+CD45RA− closely resembles the immediate precursors of pre-DC1, rapidly transforming into CD8− DCs after tumor necrosis factor-α (TNF-α) stimulation. These findings indicate the close relationship between human and mouse DCs, provided cells are obtained directly from equivalent source materials.

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12

Kvedaraite, Egle, Laura Hertwig, Indranil Sinha, Andrea Ponzetta, Ida Hed Myrberg, Magda Lourda, Majda Dzidic, et al. "Major alterations in the mononuclear phagocyte landscape associated with COVID-19 severity." Proceedings of the National Academy of Sciences 118, no. 6 (January 21, 2021): e2018587118. http://dx.doi.org/10.1073/pnas.2018587118.

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Dendritic cells (DCs) and monocytes are crucial mediators of innate and adaptive immune responses during viral infection, but misdirected responses by these cells may contribute to immunopathology. Here, we performed high-dimensional flow cytometry-analysis focusing on mononuclear phagocyte (MNP) lineages in SARS-CoV-2–infected patients with moderate and severe COVID-19. We provide a deep and comprehensive map of the MNP landscape in COVID-19. A redistribution of monocyte subsets toward intermediate monocytes and a general decrease in circulating DCs was observed in response to infection. Severe disease coincided with the appearance of monocytic myeloid-derived suppressor cell-like cells and a higher frequency of pre-DC2. Furthermore, phenotypic alterations in MNPs, and their late precursors, were cell-lineage–specific and associated either with the general response against SARS-CoV-2 or COVID-19 severity. This included an interferon-imprint in DC1s observed in all patients and a decreased expression of the coinhibitory molecule CD200R in pre-DCs, DC2s, and DC3 subsets of severely sick patients. Finally, unsupervised analysis revealed that the MNP profile, alone, pointed to a cluster of COVID-19 nonsurvivors. This study provides a reference for the MNP response to SARS-CoV-2 infection and unravels mononuclear phagocyte dysregulations associated with severe COVID-19.

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13

Eastman, Alison J., Nicole Potchen, Guolei Zhou, Jintao Xu, Lori Neal, Antoni Malachowski, Steven L. Kunkel, Ilona Kryczek, John J. Osterholzer, and Michal A. Olszewski. "Early TNFα signaling results in pulmonary DC1 polarization and programing of murine myeloid precursor cells in the bone marrow towards DC1 polarization throughout Cryptococcus neoformans infection." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 126.10. http://dx.doi.org/10.4049/jimmunol.196.supp.126.10.

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Abstract TNFα is required for protective Th1/Th17 immunity to Cryptococcus neoformans (CN), an opportunistic pulmonary fungal pathogen. The effects of TNFα are linked to the stable, early classical activation of dendritic cells (DC1), preventing alternative (DC2) activation. We hypothesized that TNFα signaling facilitates epigenetic modification of key DC genes during CN infection. We tested this hypothesis using CBA/J mice infected intratracheally with CN and injected once on day 0 intraperitoneally with control or a TNFα-depleting antibody (αTNFα). αTNFα mice had no difference in pulmonary CFU at 7 days post-infection (dpi), but had significantly higher fungal burden and extrapulmonary dissemination at 14 and 28 dpi. DCs from the lungs of control mice at 7 dpi had increased association of iNOS and IL-12b promoters with the activating modification histone 3 lysine 4 trimethylation (H3K4me3), while DCs from αTNFα mice did not. Because DCs have a relatively short half-life during infection, we assessed the bone marrow (BM) myeloid precursor cells (MPCs) from infected animals with and without TNFα. Intranuclear flow cytometry for H3K4me3 showed distinct patterns of global trimethylation between infected control and αTNFα mice as early as 7 dpi. We next tested whether BM-derived DCs (BMDCs) matured ex vivo from infected animals would yield DC1 or DC2 cells. BMDCs from control animals became DC1, and resisted changes to polarization when challenged with the DC2-skewing IL-4, while BMDCs matured from TNFα-depleted mice maintained DC2 polarization when challenged with IFNγ. We conclude that TNFα epigenetically modifies key DC1 genes in MPCs, thereby sustaining lasting DC1 programing of DCs required for clearance of CN from the infected lungs.

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14

Schmitz, Marc, Senming Zhao, Yvonne Deuse, Knut Schaekel, Martin Bornhaeuser, and Peter Rieber. "Tumoricidal Potential of Native Human Blood Dendritic Cells: Direct Tumor Cell Killing and Activation of NK Cell-Mediated Cytotoxicity." Blood 104, no. 11 (November 16, 2004): 449. http://dx.doi.org/10.1182/blood.v104.11.449.449.

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Abstract Dendritic cells (DCs) are characterized by their unique capacity for primary T cell activation, providing the opportunity of DC-based cancer vaccination protocols. Recently, we defined a novel major subset of human blood DCs by using the monoclonal antibody M-DC8 which recognizes a carbohydrate modification of P selectin glycoprotein ligand-1 (PSGL-1) selectively expressed on these cells (Immunity2002;17:289-301). In addition to a marked capacity to activate tumor-reactive cytotoxic T cells M-DC8+ DCs efficiently mediate antibody-dependent cytotoxicity (Blood;2002;100:1502-1504). In the present study, we analyzed the capacity of M-DC8+ DCs to kill tumor cells in the absence of antibodies and to enhance the tumor-directed cytotoxicity of NK cells. To determine whether M-DC8+ DCs exhibit tumoricidal activity, DCs were isolated at high purity (>93%) from the blood of healthy donors by immunomagnetic separation. These cells were cultured for 6 h in the presence or absence of 200 U/ml interferon (IFN)-gamma. Subsequently, DCs were coincubated with four chromium-labeled tumor cell lines and two normal cell lines for 18 h. Whereas unstimulated DCs demonstrated only moderate tumor-directed cytotoxicity (specific lysis: 7–13%), IFN-gamma-stimulated M-DC8+ DCs displayed potent killing of each of these tumor cell lines (specific lysis: 27–35%). Only a marginal cytotoxic effect was seen when normal human cells such as lung fibroblasts or endothelial cells were used as targets. When evaluating the cytotoxic effector mechanisms FACS analysis and ELISA assays revealed that IFN-gamma-stimulated M-DC8+ DCs secreted a high amount of tumor necrosis factor (TNF)-alpha induced by direct cell-to-cell contact with the different tumor cell lines. This effect was already observed after 3 h of cocultivation. Interestingly, no significant induction of TNF-alpha was detected during contact of M-DC8+ DCs with the normal human cell lines. These results suggest that tumor-associated surface molecules are important for the observed increase of TNF-alpha production in M-DC8+ DCs. Inhibition experiments with neutralizing antibodies clearly demonstrated that tumor cell-induced TNF-alpha play an important role in tumor-directed cytotoxicity mediated by M-DC8+ DCs. To investigate whether M-DC8+ DCs enhance the tumoricidal activity of NK cells freshly isolated DCs were cultured for 6 h in the presence or absence of IFN-gamma. Thereafter, DCs were coincubated with highly enriched (>90%) NK cells. The cytotoxic potential of the stimulated NK cells was tested towards various tumor cell lines in a 4 h chromium release assay. We observed a two- to threefold increase of NK cell-mediated cytotoxicity towards all analyzed tumor cell lines by IFN-gamma-stimulated M-DC8+ DCs. In addition, transwell experiments demonstrated that this triggering effect was mainly dependent on cell-to-cell contact. In conclusion, our data provide evidence that a major subpopulation of circulating human blood DCs exhibits efficient tumoricidal activity and clearly enhances NK cell-mediated tumor-directed cytotoxicity. The capacity of DCs to induce tumor-specific T cell responses and to kill tumor cells either directly or by activating NK cells points to the pivotal role of DCs in triggering the innate and adaptive immune response against tumors.

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15

Klangsinsirikul, Phennapha, G. Ian Carter, Jennifer L. Byrne, Geoff Hale, and Nigel H. Russell. "Campath-1G causes rapid depletion of circulating host dendritic cells (DCs) before allogeneic transplantation but does not delay donor DC reconstitution." Blood 99, no. 7 (April 1, 2002): 2586–91. http://dx.doi.org/10.1182/blood.v99.7.2586.

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Graft-versus-host disease (GVHD), a major complication after allogeneic transplantation, can be abrogated by the Campath (anti-CD52) monoclonal antibody. The induction of acute GVHD requires host antigens to be presented to donor T cells by antigen-presenting cells (APCs). Recent evidence has suggested that only host APCs can interact with donor T cells in the induction of GVHD. Because CD52 has been reported to be expressed on DCs, we reasoned that pretransplant Campath-1G might have a direct effect on circulating DCs in addition to any effects on donor T cells. Using direct immunostaining, we demonstrated expression of CD52 on DCs and that Campath-1G killed purified DCs in vitro. In vivo Campath also depleted DCs. Twenty-four hours after the first dose of Campath-1G, circulating DCs were reduced by a mean of 79% (range, 44%-96%). By day 0 after 5 doses of Campath-1G and chemoradiotherapy conditioning, DCs became undetectable in 7 of 9 cases, whereas in 6 of 7 patients receiving conditioning therapy without Campath-1G, host DCs were still detectable. The reconstitution of circulating DCs after transplantation was not affected by Campath-1G and in both groups DC1 (CD11c+) recovered more rapidly than DC2 (CD11c−). Analysis of chimerism confirmed that the DCs recovering after transplantation in patients receiving Campath-1G were of donor origin. We conclude that in vivo Campath-1G causes a rapid depletion of host circulating DCs and that this may, in part, explain the low incidence of acute GVHD. The reconstitution of donor DCs was not delayed, which may be important in preserving immune reconstitution.

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16

Plantinga, Maud, Denise A. M. H. van den Beemt, Ester Dünnebach, and Stefan Nierkens. "CD14 Expressing Precursors Give Rise to Highly Functional Conventional Dendritic Cells for Use as Dendritic Cell Vaccine." Cancers 13, no. 15 (July 29, 2021): 3818. http://dx.doi.org/10.3390/cancers13153818.

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Induction of long-lasting immunity by dendritic cells (DCs) makes them attractive candidates for anti-tumor vaccination. Although DC vaccinations are generally considered safe, clinical responses remain inconsistent in clinical trials. This initiated studies to identify subsets of DCs with superior capabilities to induce effective and memory anti-tumor responses. The use of primary DCs has been suggested to overcome the functional limitations of ex vivo monocyte-derived DCs (moDC). The ontogeny of primary DCs has recently been revised by the introduction of DC3, which phenotypically resembles conventional (c)DC2 as well as moDC. Previously, we developed a protocol to generate cDC2s from cord blood (CB)-derived stem cells via a CD115-expressing precursor. Here, we performed index sorting and single-cell RNA-sequencing to define the heterogeneity of in vitro developed DC precursors and identified CD14+CD115+ expressing cells that develop into CD1c++DCs and the remainder cells brought about CD123+DCs, as well as assessed their potency. The maturation status and T-cell activation potential were assessed using flow cytometry. CD123+DCs were specifically prone to take up antigens but only modestly activated T-cells. In contrast, CD1c++ are highly mature and specialized in both naïve as well as antigen-experienced T-cell activation. These findings show in vitro functional diversity between cord blood stem cell-derived CD123+DC and CD1c++DCs and may advance the efficiency of DC-based vaccines.

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17

Ferris, Stephen T., Vivek Durai, Renee Wu, Theresa L. Murphy, and Kenneth M. Murphy. "Batf3-dependent Dendritic Cells are Required to Present Cell-associated Antigen to CD4 T Cells." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 177.33. http://dx.doi.org/10.4049/jimmunol.202.supp.177.33.

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Abstract Dendritic cells (DCs) are required to prime T cells during an immune response. The dogma in the field is that Batf3-dependent DCs (DC1s) prime CD8 T cells and IRF4-dependent DCs (DC2s) prime CD4 T cells. However, recent studies have shown that DC1s are required for induction of Th1 immune responses and to prime autroreactive CD4 T cells in the NOD mouse model of diabetes. Therefore, this segregation of priming theory is flawed. To further study the contribution of DC1s to CD4 T cell priming, we generated an XCR1-cre mouse and crossed it to the MHC class II floxed mouse to generate MHC class II deficient DC1s. We found that the form of antigen directs the priming of T cells. DC2s are superior at presenting soluble antigen as evidenced by normal CD4 and CD8 OVA specific T cell responses in mice lacking DC1s. However, DC1s are superior at presenting cell-associated antigen as evidenced by a lack of OVA specific CD4 and CD8 T cell priming in mice lacking DC1s. Furthermore, CD4 priming during tumor immune responses is absent when DC1s lack MHC class II. Our findings show that the DC subsets differ in the form of antigen that they present. DC1s present cell-associated material; whereas DC2s present soluble antigen.

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18

Van Epps, Heather L. "Melanomas disable DCs." Journal of Experimental Medicine 203, no. 7 (June 26, 2006): 1621a. http://dx.doi.org/10.1084/jem.2037iti2.

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Bashyam, Hema. "Tumor-killing DCs." Journal of Experimental Medicine 204, no. 6 (May 29, 2007): 1241. http://dx.doi.org/10.1084/jem.2046iti3.

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20

Parker, Stephen. "ICTs and DCs." Information Development 22, no. 3 (August 2006): 155–56. http://dx.doi.org/10.1177/0266666906068812.

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21

Dempsey, Laurie A. "Fate-mapping DCs." Nature Immunology 14, no. 10 (September 18, 2013): 1023. http://dx.doi.org/10.1038/ni.2718.

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22

Dempsey, Laurie A. "lncRNA for DCs." Nature Immunology 15, no. 6 (May 19, 2014): 530. http://dx.doi.org/10.1038/ni.2903.

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23

Brassard, Julyanne, Emilie Bernatchez, Anick Langlois, and Marie-Renée Blanchet. "CD103 expression by DCs: a new player in lung cancer immunity." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 56.21. http://dx.doi.org/10.4049/jimmunol.200.supp.56.21.

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Abstract Despite the use of various therapies, lung cancer remains one of the world’s leading causes of death. Cancer immunotherapy is a promising therapeutic avenue, however, molecular and cellular mechanisms involved in cancer immunity remain elusive. Dendritic cells (DCs), which play an important role in CD8+ T cell activation in cancer immunity, can be divided into two major populations, namely DC1 and DC2, and respectively identified by XCR1/CD103 and Sirpα/CD11b expression. Importantly, studies have demonstrated that DC1s promote cancer immune responses. Furthermore, CD103+ DC1s specialize in the transport of tumor antigens to draining lymph nodes and cross-presentation. However, the influence of the cancer environment, where inflammatory factors (such as TNF) and various inflammatory cells are found, on CD103 expression by DC has never been studied. To verify whether lung cancer-induced inflammation modulates CD103 DC population, fresh lung and splenic DCs were isolated in wild type (WT) mice and exposed to GM-CSF (a known inducer of CD103 expression in the lung) with or without TNF. Furthermore, to directly assess the impact of lung cancer on CD103 DC expression, WT mice were euthanized 2 and 3 weeks following intravenous injection of Lewis lung carcinoma (LLC) cells and the percentage of CD103+DC1 was analyzed in lungs. Exposure to TNF blocked the GM-CSF-induced CD103 expression by DCs, independently of the timing at which TNF is added to cultures (before or after GM-CSF). Also, the % of CD103+ DCs gradually decreased in time following LLC injection. This suggests a new mechanism by which lung cancer negatively impacts the function of immune cells to promote cancer development, and could lead to new therapeutic avenues in cancer immunity.

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Fujii, Jun. "DCS Evolution ^|^ldquo;The Next Generation DCS. Experion PKS^|^rdquo;." JAPAN TAPPI JOURNAL 67, no. 11 (2013): 1295–98. http://dx.doi.org/10.2524/jtappij.67.1295.

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25

Novais, Cândido Barreto de, and José Oswaldo Siqueira. "Aplicação de formononetina na colonização e esporulação de fungos micorrízicos em braquiária." Pesquisa Agropecuária Brasileira 44, no. 5 (May 2009): 496–502. http://dx.doi.org/10.1590/s0100-204x2009000500009.

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O objetivo deste trabalho foi avaliar o efeito de aplicações de Mycoform na colonização micorrízica e esporulação de 13 isolados de fungos micorrízicos arbusculares em Brachiaria decumbens. O experimento foi conduzido em casa de vegetação, em solo esterilizado, com delineamento experimental inteiramente casualizado, em arranjo fatorial 3x13, com cinco repetições. O produto foi aplicado no plantio e foi ou não aplicado uma segunda vez 60 dias depois, na quantidade de 2 mg kg-1 de solo. Aos 150 dias de crescimento das plantas, foram coletadas amostras de raízes e de solo rizosférico, para a avaliação de colonização radicular e densidade de esporos. Houve estímulo do Mycoform nos parâmetros avaliados, efeito que variou com os isolados estudados. Foi observado efeito significativo da aplicação do Mycoform na colonização das raízes pelos isolados Glomus clarum DCS 09 e DCS 10, Paraglomus occultum DCS 06 e Acaulospora delicata DCS 02 e na esporulação dos isolados G. clarum DCS 09 e DCS 10, P. occultum DCS 06 e DCS 31, Glomus etunicatum DCS 12, A. delicata DCS 30 e Kuklospora colombiana DCS 03. O incremento na esporulação atingiu 89% e, na colonização, 60%, o que confirma os benefícios da formononetina na colonização e na esporulação dos fungos micorrízicos arbusculares.

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26

Howle, Laurens E., Paul W. Weber, Richard D. Vann, and Mark C. Campbell. "Marginal DCS events: their relation to decompression and use in DCS models." Journal of Applied Physiology 107, no. 5 (November 2009): 1539–47. http://dx.doi.org/10.1152/japplphysiol.00185.2009.

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We consider the nature and utility of marginal decompression sickness (DCS) events in fitting probabilistic decompression models to experimental dive trial data. Previous works have assigned various fractional weights to marginal DCS events, so that they contributed to probabilistic model parameter optimization, but less so than did full DCS events. Inclusion of fractional weight for marginal DCS events resulted in more conservative model predictions. We explore whether marginal DCS events are correlated with exposure to decompression or are randomly occurring events. Three null models are developed and compared with a known decompression model that is tuned on dive trial data containing only marginal DCS and non-DCS events. We further investigate the technique by which marginal DCS events were previously included in parameter optimization, explore the effects of fractional weighting of marginal DCS events on model optimization, and explore the rigor of combining data containing full and marginal DCS events for probabilistic DCS model optimization. We find that although marginal DCS events are related to exposure to decompression, empirical dive data containing marginal and full DCS events cannot be combined under a single DCS model. Furthermore, we find analytically that the optimal weight for a marginal DCS event is 0. Thus marginal DCS should be counted as no-DCS events when probabilistic DCS models are optimized with binomial likelihood functions. Specifically, our study finds that inclusion of marginal DCS events in model optimization to make the dive profiles more conservative is counterproductive and worsens the model's fit to the full DCS data.

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27

Ngoi, Soo M., Yi Yang, Stephen Iwanowycz, Jennifer Gutierrez, Megan Hill, Carter Allen, Dongjun Chung, and Bei Liu. "Migratory type 2 dendritic cells mediate mucosal Th17 response to gut commensal bacteria." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 115.02. http://dx.doi.org/10.4049/jimmunol.208.supp.115.02.

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Abstract Dendritic cells (DCs) are professional antigen-presenting cells equipped with MHC-restricted antigens, co-stimulations, and cytokines that effectively prime and differentiate naïve T cells into distinct functional subsets. The immune signals that DCs carry reflect the route of antigen uptake and the innate stimuli they received. In the mucosal tissues, owing to the great variety of foreign antigens and inflammatory cues, DCs are predominantly activated and migratory. The gut commensal bacteria contribute to immune health by educating the immune system at this unique location interfacing with the outside environment. In the small intestine, CD4 Th17 cells are abundant and play a critical role in mucosal defense against bacterial and fungal infections. We identified that the early priming step of commensal-driven Th17 cells is controlled by bona fide Zbtb46-expressing DCs. CCR7-dependent migration of DC2s from the small intestine to the mesenteric lymph nodes is essential for the activation of naïve CD4 T cells. The migratory DC2 population in the MLN are almost exclusively Esam+ cells. Single-cell RNA sequencing highlighted the abundance of co-stimulatory markers (CD40 and OX40) and chemokines (Ccl22 and Cxcl16) on MLN migratory DCs. Further resolution of MLN migratory DC2s revealed that the Th17-polarizing cytokine IL-6 colocalizes with DC2s expressing CD40, Ccl17, and Ccl22. Our study indicates that the mucosal Th17 cell response is regulated by a restricted subset of migratory DC2s in the gut draining lymph nodes. Supported by NIAID U01AI125859

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28

Faries, Mark B., Isabelle Bedrosian, Shuwen Xu, Gary Koski, James G. Roros, Mirielle A. Moise, Hung Q. Nguyen, Friederike H. C. Engels, Peter A. Cohen, and Brian J. Czerniecki. "Calcium signaling inhibits interleukin-12 production and activates CD83+ dendritic cells that induce Th2 cell development." Blood 98, no. 8 (October 15, 2001): 2489–97. http://dx.doi.org/10.1182/blood.v98.8.2489.

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Abstract Mature dendritic cells (DCs), in addition to providing costimulation, can define the Th1, in contrast to the Th2, nature of a T-cell response through the production of cytokines and chemokines. Because calcium signaling alone causes rapid DC maturation of both normal and transformed myeloid cells, it was evaluated whether calcium-mobilized DCs polarize T cells toward a Th1 or a Th2 phenotype. After human monocytes were cultured for 24 hours in serum-free medium and granulocyte-macrophage colony-stimulating factor to produce immature DCs, additional overnight culture with either calcium ionophore (CI) or interferon γ (IFN-γ), tumor necrosis factor-α (TNF-α), and soluble CD40L resulted in phenotypically mature DCs that produced interleukin-8 (IL-8) and displayed marked expression of CD80, CD86, CD40, CD54, CD83, DC-LAMP, and RelB. DCs matured by IFN-γ, TNF-α, and soluble CD40L were additionally distinguished by undetectable CD4 expression, marked secretion of IL-12, IL-6, and MIP-1β, and preferential ability to promote Th1/Tc1 characteristics during T-cell sensitization. In contrast, DCs matured by CI treatment were distinguished by CD4 expression, modest or absent levels of IL-12, IL-6, and MIP-1β, and preferential ability to promote Th2/Tc2 characteristics. Calcium signaling selectively antagonized IL-12 production by mature DCs activated with IFN-γ, TNF-α, and soluble CD40L. Although the activation of DCs by calcium signals is largely mediated through calcineurin phosphatase, the inhibition of IL-12 production by calcium signaling was independent of this enzyme. Naturally occurring calcium fluxes in immature DCs, therefore, negatively regulate Dc1 differentiation while promoting Dc2 characteristics and Th2/Tc2 polarization. Calcium-mobilized DCs may have clinical usefulness in treating disease states with excessive Th1/Tc1 activity, such as graft-versus-host disease or autoimmunity.

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29

Schmitz, Marc, Senming Zhao, Knut Schäkel, Martin Bornhäuser, Detlef Ockert, and Ernst Peter Rieber. "Native human blood dendritic cells as potent effectors in antibody-dependent cellular cytotoxicity." Blood 100, no. 4 (August 15, 2002): 1502–4. http://dx.doi.org/10.1182/blood.v100.4.1502.h81602001502_1502_1504.

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Functional studies on native human dendritic cells (DCs) are hampered by technical difficulties in preparing fresh DCs. Recently, with the help of the monoclonal antibody M-DC8, we succeeded in isolating a major subpopulation of human blood DCs by a one-step immunomagnetic separation procedure. These cells strongly express FcγRIII (CD16) and FcγRII (CD32) and are quite efficient in the antigen-specific activation of naive T cells. Because some Fcγ receptor-bearing cell types are known as effector cells in antibody-dependent cellular cytotoxicity (ADCC), we investigated whether M-DC8+ DCs are capable of effectuating ADCC. In this report we show that freshly prepared M-DC8+ DCs efficiently mediate tumor-directed ADCC and that both types of Fcγ receptors as well as tumor necrosis factor α essentially contribute to the cytotoxic activity. The results provide evidence that, in addition to their pivotal role in primary T-cell activation, a subset of blood DCs displays efficient cytotoxicity in ADCC.

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Ghosh, DK, C. Kodange, CS Mohanty, and Rohit Verma. "Decompression sickness (DCS) and diving illnesses mimicking DCS : A case series." Journal of Marine Medical Society 18, no. 1 (2016): 40. http://dx.doi.org/10.4103/0975-3605.202979.

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31

Tsarouchas, C., S. Schlenker, G. Dimitrov, and G. Jahn. "Dcs Data Viewer, an Application that Accesses ATLAS DCS Historical Data." Journal of Physics: Conference Series 513, no. 3 (June 11, 2014): 032097. http://dx.doi.org/10.1088/1742-6596/513/3/032097.

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32

Yoneyama, Hiroyuki, Kenjiro Matsuno, Etsuko Toda, Tetsu Nishiwaki, Naoki Matsuo, Akiko Nakano, Shosaku Narumi, et al. "Plasmacytoid DCs help lymph node DCs to induce anti-HSV CTLs." Journal of Experimental Medicine 202, no. 3 (August 1, 2005): 425–35. http://dx.doi.org/10.1084/jem.20041961.

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Antiviral cell–mediated immunity is initiated by the dendritic cell (DC) network in lymph nodes (LNs). Plasmacytoid DCs (pDCs) are known to migrate to inflamed LNs and produce interferon (IFN)-α, but their other roles in antiviral T cell immunity are unclear. We report that LN-recruited pDCs are activated to create local immune fields that generate antiviral cytotoxic T lymphocytes (CTLs) in association with LNDCs, in a model of cutaneous herpes simplex virus (HSV) infection. Although pDCs alone failed to induce CTLs, in vivo depletion of pDCs impaired CTL-mediated virus eradication. LNDCs from pDC-depleted mice showed impaired cluster formation with T cells and antigen presentation to prime CTLs. Transferring circulating pDC precursors from wild-type, but not CXCR3-deficient, mice to pDC-depleted mice restored CTL induction by impaired LNDCs. In vitro co-culture experiments revealed that pDCs provided help signals that recovered impaired LNDCs in a CD2- and CD40L-dependent manner. pDC-derived IFN-α further stimulated the recovered LNDCs to induce CTLs. Therefore, the help provided by pDCs for LNDCs in primary immune responses seems to be pivotal to optimally inducing anti-HSV CTLs.

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33

Mitchell, Simon J. "DCS or DCI? The difference and why it matters." Diving and Hyperbaric Medicine Journal 49, no. 3 (September 30, 2019): 152–53. http://dx.doi.org/10.28920/dhm49.3.152-153.

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34

Parida, Sasmita, Bibudhendu Pati, Suvendu Nayak, Chhabi Panigrahi, and Tien-Hsiung Weng. "PE-DCA: Penalty elimination based data center allocation technique using guided local search for IaaS cloud." Computer Science and Information Systems, no. 00 (2021): 59. http://dx.doi.org/10.2298/csis210512059p.

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In Cloud computing the user requests are passaged to data centers (DCs) to accommodate resources. It is essential to select the suitable DCs as per the user requests so that other requests should not be penalized in terms of time and cost. The searching strategies consider the execution time rather than the related penalties while searching DCs. In this work, we discuss Penalty Elimination-based DC Allocation (PE-DCA) using Guided Local Search (GLS) mechanism to locate suitable DCs with reduced cost, response time, and processing time. The PE-DCA addresses, computes, and eliminates the penalties involved in the cost and time through iterative technique using the defined objective and guide functions. The PE-DCA is implemented using CloudAnalyst with various configurations of user requests and DCs. We examine the PE-DCA and the execution after-effects of various costs and time parameters to eliminate the penalties and observe that the proposed mechanism performs best.

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35

Ferrarelli, Leslie K. "Putting DCs into overdrive." Science 372, no. 6541 (April 29, 2021): 476.8–477. http://dx.doi.org/10.1126/science.372.6541.476-h.

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36

Bird, Lucy. "Gremlin neighbours for DCs." Nature Reviews Immunology 21, no. 6 (May 14, 2021): 344–45. http://dx.doi.org/10.1038/s41577-021-00565-4.

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37

Takayama, Takekazu. "New Trials Surrounding DCS." JAPAN TAPPI JOURNAL 57, no. 3 (2003): 338–45. http://dx.doi.org/10.2524/jtappij.57.338.

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38

Da Silva, Kevin. "Vaccine stresses out DCs." Nature Medicine 20, no. 1 (January 2014): 28. http://dx.doi.org/10.1038/nm.3455.

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39

Van Epps, Heather L. "Can DCs forecast atherosclerosis?" Journal of Experimental Medicine 203, no. 9 (August 7, 2006): 2045a. http://dx.doi.org/10.1084/jem.2039iti1.

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40

Robinson, Richard. "Skin DCs go deeper." Journal of Experimental Medicine 204, no. 13 (December 17, 2007): 3054. http://dx.doi.org/10.1084/jem.20413iti3.

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41

Robinson, Richard. "Skin DCs go deeper." Journal of Experimental Medicine 205, no. 1 (December 24, 2007): 257. http://dx.doi.org/10.1084/jem.20413iti3121907c.

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42

Maxmen, Amy. "Giving gut DCs personality." Journal of Experimental Medicine 206, no. 9 (August 24, 2009): 1834–35. http://dx.doi.org/10.1084/jem.2069iti3.

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43

Mishra, Sanjat, and Nitaigour Mahalik. "Virtual DCS and specification." International Journal of Information and Communication Technology 3, no. 4 (2011): 339. http://dx.doi.org/10.1504/ijict.2011.043629.

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44

Bell, Jennifer. "DCs out of control." Nature Reviews Immunology 1, no. 3 (December 2001): 171. http://dx.doi.org/10.1038/35105036.

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45

Wang, Jiongkun, and Feiyue Xing. "Human TSLP-Educated DCs." Cellular & Molecular Immunology 5, no. 2 (April 2008): 99–106. http://dx.doi.org/10.1038/cmi.2008.12.

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46

Alderton, Gemma K. "TIM3 suppresses antitumour DCs." Nature Reviews Cancer 12, no. 9 (August 24, 2012): 584. http://dx.doi.org/10.1038/nrc3349.

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47

&NA;. "DCs Favored Over GPs." Back Letter 8, no. 1 (1993): 1. http://dx.doi.org/10.1097/00130561-199308010-00002.

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48

Vari, F., and D. N. J. Hart. "Loading DCs with Ag." Cytotherapy 6, no. 2 (April 2004): 111–21. http://dx.doi.org/10.1080/14653240410005230.

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Matsushima, Hironori, and Akira Takashima. "Cyclophosphamide, DCs, and Tregs." Blood 115, no. 22 (June 3, 2010): 4322–24. http://dx.doi.org/10.1182/blood-2010-03-273409.

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50

Fehervari, Zoltan. "HIV keeps DCs immature." Nature Immunology 16, no. 6 (May 19, 2015): 590. http://dx.doi.org/10.1038/ni.3184.

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