Relevant bibliographies by topics / Regulatory DC

Academic literature on the topic 'Regulatory DC'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Regulatory DC"

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Via, Steve H. "DC Beat -- Drinking Water Regulatory Priorities." Journal - American Water Works Association 109 (May 1, 2017): 88–91. http://dx.doi.org/10.5942/jawwa.2017.109.0067.

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Barchet, Winfried, Jeffrey D. Price, Marina Cella, Marco Colonna, Sandra K. MacMillan, J. Perren Cobb, Paul A. Thompson, Kenneth M. Murphy, John P. Atkinson, and Claudia Kemper. "Complement-induced regulatory T cells suppress T-cell responses but allow for dendritic-cell maturation." Blood 107, no. 4 (February 15, 2006): 1497–504. http://dx.doi.org/10.1182/blood-2005-07-2951.

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Concurrent activation of the T-cell receptor (TCR) and complement regulator CD46 on human CD4+ T lymphocytes induces Tr1-like regulatory T cells that suppress through IL-10 secretion bystander T-cell proliferation. Here we show that, despite their IL-10 production, CD46-induced T-regulatory T cells (Tregs) do not suppress the activation/maturation of dendritic cells (DCs). DC maturation by complement/CD46-induced Tregs is mediated through simultaneous secretion of GM-CSF and soluble CD40L, factors favoring DC differentiation and reversing inhibitory effects of IL-10. Thus, CD46-induced Tregs produce a distinct cytokine profile that inhibits T-cell responses but leaves DC activation unimpaired. Such “DC-sparing” Tregs could be desirable at host/environment interfaces such as the gastrointestinal tract where their specific cytokine profile provides a mechanism that ensures unresponsiveness to commensal bacteria while maintaining reactivity to invading pathogens.
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Diao, Jun, Anastassia Mikhailova, Michael Tang, Hongtao Gu, Jun Zhao, and Mark S. Cattral. "Immunostimulatory conventional dendritic cells evolve into regulatory macrophage-like cells." Blood 119, no. 21 (May 24, 2012): 4919–27. http://dx.doi.org/10.1182/blood-2011-11-392894.

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Abstract Dendritic cell (DC) homeostasis in peripheral tissues reflect a balance between DC generation, migration, and death. The current model of DC ontogeny indicates that pre-cDCs are committed to become terminal conventional DCs (cDCs). Here, we report the unexpected finding that proliferating immunostimulatory CD11c+ MHC class II+ cDCs derived from pre-cDCs can lose their DC identity and generate progeny that exhibit morphologic, phenotypic, and functional characteristics of regulatory macrophages. DC-derived–macrophages (DC-d-Ms) potently suppress T-cell responses through the production of immunosuppressive molecules including nitric oxide, arginase, and IL-10. Relative deficiency of granulocyte-macrophage colony stimulating factor (GM-CSF) provided a permissive signal for DC-d-M generation. Using a transgenic mouse model that allows tracking of CD11c+ cells in vivo, we found that DC-d-M development occurs commonly in cancer, but not in lymphoid or nonlymphoid tissues under steady-state conditions. We propose that this developmental pathway serves as an alternative mechanism of regulating DC homeostasis during inflammatory processes.
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Poncini, Carolina Verónica, Catalina Dirney Alba Soto, Estela Batalla, Maria Elisa Solana, and Stella Maris González Cappa. "Trypanosoma cruzi Induces Regulatory Dendritic Cells In Vitro." Infection and Immunity 76, no. 6 (March 17, 2008): 2633–41. http://dx.doi.org/10.1128/iai.01298-07.

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ABSTRACT A main feature of acute infection with Trypanosoma cruzi is the presence of immunological disorders. A previous study demonstrated that acute infection with the virulent RA strain downregulates the expression of major histocompatibility complex class II (MHC-II) on antigen-presenting cells and impairs the T-cell stimulatory capacity of splenic dendritic cells (DC). In the present work, we assessed the ability of trypomastigotes (Tp) to modulate the differentiation stage and functionality of bone marrow-derived DC in vitro. We observed that the Tp stage of T. cruzi failed to activate DC, which preserved their low expression of MHC-II and costimulatory molecules, as well as their endocytic activity. We also show that Tp induced transforming growth factor β (TGF-β) secretion by DC and enhanced the gap between interleukin-10 (IL-10) and IL-12p70 production, showing a higher IL-10/IL-12p70 ratio upon lipopolysaccharide (LPS) treatment. In addition, we observed that Tp prevented DC full activation induced by LPS, thereby downregulating their MHC-II surface expression and inhibiting their capacity to stimulate lymphocyte proliferation. In vitro IL-10 neutralization during the differentiation process of DC with Tp+LPS showed a reversion of their inhibitory effect during mixed lymphocyte reaction. In contrast, only simultaneous neutralization of IL-10 and TGF-β, after DC differentiation, was involved in the partial restitution of lymphocyte proliferation. Since both TGF-β and IL-10 are immunosuppressive cytokines essential in the modulation of the immune response and important in the induction of tolerance, our results suggest for the first time that Tp are responsible for the generation of regulatory DC in vitro.
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Johnson, Jarrod S., Nicholas De Veaux, Alexander W. Rives, Xavier Lahaye, Sasha Y. Lucas, Brieuc Pérot, Marine Luka, et al. "A comprehensive map of the human dendritic cell HIV-response transcriptional network." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 75.11. http://dx.doi.org/10.4049/jimmunol.202.supp.75.11.

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Abstract Transcriptional programming of the innate immune response is pivotal for host protection. However, the transcriptional mechanisms that link pathogen sensing with innate activation remain poorly understood. During infection with HIV-1, human dendritic cells (DCs) can detect the virus through an innate sensing pathway leading to antiviral type I interferon and DC maturation. Here, we have developed an iterative experimental and computational approach to map the innate response circuitry during HIV-1 infection. By integrating genome-wide chromatin accessibility with expression kinetics, we have inferred a gene regulatory network that links 542 transcription factors (TFs) with 21,862 target genes. Through genetic perturbation and drug treatments we identify PRDM1 and RARA as essential regulators of the interferon response and DC maturation, respectively. Our work provides a resource for interrogation of regulators of HIV replication and innate immunity, highlighting the complexity and cooperativity in the regulatory circuit controlling the DC response to HIV-1 infection.
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Lipscomb, Michael W., Jennifer L. Taylor, Cristina J. Goldbach, Simon C. Watkins, Amy K. Wesa, and Walter J. Storkus. "DC expressing transgene Foxp3 are regulatory APC." European Journal of Immunology 40, no. 2 (February 2010): 480–93. http://dx.doi.org/10.1002/eji.200939667.

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Huang, Gonghua, Yanyan Wang, and Hongbo Chi. "TAK1-dependent checkpoint in dendritic cell survival promotes immune homeostasis and function (111.53)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 111.53. http://dx.doi.org/10.4049/jimmunol.188.supp.111.53.

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Abstract Homeostatic control of dendritic cell (DC) survival is crucial for adaptive immunity, but the molecular mechanism is not well defined. Moreover, how DCs influence immune homeostasis under steady state remains unclear. Combining DC-specific and inducible deletion systems, we report that the kinase TAK1 is an essential regulator of DC survival and immune system homeostasis and function. Deficiency of TAK1 in CD11c+ cells induced markedly elevated apoptosis, leading to the depletion of DC populations, especially the CD8+ and CD103+ DC subsets in lymphoid and non-lymphoid tissues, respectively. TAK1 also contributed to DC development by promoting the generation of DC precursors. Pro-survival signals from Toll-like receptors, CD40 and RANK are integrated by TAK1 in DCs, which in turn mediated activation of downstream NFκ-B and AKT-Foxo pathways and established a gene-expression program. TAK1 deficiency in DCs caused a myeloid proliferative disorder characterized by expansion of neutrophils and inflammatory monocytes, disrupted T cell homeostasis, and prevented effective T cell priming and generation of regulatory T cells. Moreover, TAK1 signaling in DCs was required to prevent myeloid proliferation even in the absence of lymphocytes, indicating a previously unappreciated regulatory mechanism of DC-mediated control of myeloid cell-dependent inflammation. Therefore, TAK1 orchestrates a pro-survival checkpoint in DCs that affects the homeostasis and function of the immune system.
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Rosborough, Brian, Dàlia Raïch-Regué, Benjamin Matta, Keunwook Lee, Mark Boothby, Heth Turnquist, and Angus Thomson. "Rapamycin-resistant mTORC1 restrains dendritic cell B7-H1 expression that requires IL-1β to enhance regulatory T cell induction (P1349)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 63.27. http://dx.doi.org/10.4049/jimmunol.190.supp.63.27.

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Abstract Introduction: The mammalian Target of Rapamycin (mTOR) is a central regulator of dendritic cell (DC) function that performs the catalytic activity of mTOR complex (mTORC)1 and 2. mTORC2 functions independently from mTORC1 and is resistant to inhibition by rapamycin (RAPA); however, mTORC1 has both RAPA-sensitive and -resistant outputs. Our goal was to ascertain the role of RAPA-resistant mTOR in DC. Methods: WT C57BL/6 or B7-H1-/- bone marrow-derived DC were generated with the addition of RAPA or ATP-competitive mTOR inhibitor, which blocks all mTOR signaling. DC lacking rictor, an mTORC2-specific subunit, were generated from conditional rictor KO mice. DC induction of regulatory T cells (Treg) was determined in MLR, using BALB/c CD4+CD25- T cell responders. Results and Conclusion: RAPA and mTORC2 deletion reduced DC B7-H1 expression, but ATP-competitive mTOR inhibitors enhanced B7-H1 expression. Augmented B7-H1 expression was blocked by STAT3 inhibition and correlated with reduced expression of the STAT3 negative regulator, SOCS3. DC exposed to ATP-competitive mTOR inhibitors increased Treg induction, which was dependent on DC B7-H1. IL-1β neutralization additionally reduced Treg induction by B7-H1-/- ATP-competitive mTOR inhibitor-exposed DC, suggesting that IL-1β and B7-H1 act additively to promote Treg induction by these DC. These findings establish a RAPA-resistant mTORC1 pathway that acts through SOCS3 and STAT3 to regulate DC B7-H1 expression and Treg induction.
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Li, Haiyan S., Cliff Y. Yang, Kalyan C. Nallaparaju, Huiyuan Zhang, Yong-Jun Liu, Ananda W. Goldrath, and Stephanie S. Watowich. "The signal transducers STAT5 and STAT3 control expression of Id2 and E2-2 during dendritic cell development." Blood 120, no. 22 (November 22, 2012): 4363–73. http://dx.doi.org/10.1182/blood-2012-07-441311.

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Abstract Cytokines and transcription factors play key roles in dendritic cell (DC) development, yet information about regulatory interactions between these signals remains limited. Here we show that the cytokines GM-CSF and Flt3L induce the transcriptional mediators Id2 and E2-2 and control DC lineage diversification by STAT–dependent pathways. We found that STAT5 is required for tissue CD103+ DC generation and plasmacytoid DC (pDC) suppression in steady state or response to GM-CSF. STAT5 stimulates GM-CSF–dependent expression of Id2, which controls CD103+ DC production and pDC inhibition. By contrast, pDCs, but not CD103+ DCs, are dependent on STAT3. Consistently, STAT3 stimulates Flt3L-responsive expression of the pDC regulator Tcf4 (E2-2). These data suggest that STATs contribute to DC development by controlling transcription factors involved in lineage differentiation.
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Rosborough, Brian, Ben Matta, Heth Turnquist, and Angus Thomson. "mTORC2 negatively regulates DC PD-L1 and IL-10 through SOCS3 and STAT3 (172.34)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 172.34. http://dx.doi.org/10.4049/jimmunol.188.supp.172.34.

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Abstract The mammalian Target of Rapamycin (mTOR) is a central regulator of dendritic cells (DC) that functions in two independent complexes, mTOR complex (mTORC) 1 and 2. Rapamycin (RAPA) is a selective inhibitor of mTORC1, whereas novel ATP-competitive mTORC1/2 inhibitors (Torin1) inhibit both complexes. The immunoregulatory function of RAPA-resistant mTORC2 in DC is unknown. C57BL/6, PD-L1-/-, IL-6-/-, IL-10-/-, IL-12/23p40-/-, Ebi3-/-, interferon regulatory factor (IRF)1-/-, or FoxO1/3/4-/- bone marrow cells were cultured in GM-CSF and IL-4 to generate CD11c+ DC. RAPA or Torin1 was added on d2, and LPS added on d7. DC phenotype and signaling was assessed (d8) by flow cytometry and immunoblot, respectively. While RAPA reduced PD-L1, mTORC1/2 inhibition selectively upregulated PD-L1 expression on DC in a STAT3-dependent manner in unstimulated and LPS-stimulated DC. Whereas RAPA reduced IL-10 secretion, mTORC1/2 inhibition augmented IL-10 secretion following LPS stimulation. The PD-L1 regulator, IRF1, and FoxO, a STAT3 regulator, were not required for PD-L1 upregulation. PD-L1 upregulation on mTORC1/2-inhibited DC did not require autocrine IL-6, IL-10, IL-12/23, or IL-27. SOCS3, a negative regulator of STAT3, was reduced dramatically in mTORC1/2-inhibited, but not RAPA-exposed DC. mTORC2 negatively regulates STAT3 in DC through SOCS3. Blockade of mTORC2 signaling enhances PD-L1 expression and IL-10 secretion. These novel findings establish mTORC2 as a key regulator of DC function.
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Dissertations / Theses on the topic "Regulatory DC"

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COMI, MICHELA. "Unravelling the fingerprint and regulatory functions of human tolerogenic DC-10." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2016. http://hdl.handle.net/10281/137397.

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Dendritic cells (DC) are critically involved in initiating adaptive immune responses but they also play a pivotal role in promoting and maintaining tolerance. We identified DC-10, a subset of human tolerogenic DC characterized by the ability to produce high levels of IL-10. DC-10 can be generated in vitro from monocytes in the presence of IL-10 and are currently used for generating CD4+ T regulatory type 1 (Tr1) cells for Treg cell-based therapies. The aims of my PhD project are: 1)To define the molecular signature of DC-10; 2)To investigate modulation of in vitro and in vivo allogeneic T cell responses by DC-10. To achieve the first aim, we compared DNA microarray-based transcriptional profiling of in vitro generated DC-10 and of immunogenic mature (mDC) or immature DC (iDC). DC-10 display a molecular signature of immuno-modulation and anti-inflammation with up-regulated IL-10- and Tissue Growth Factor (TGF) beta-dependent pathways, and down-modulated signaling of pro-inflammatory cytokines. Moreover, DC-10 have an interesting matrix remodeling profile that places them as hypothetical determinants of the tolerogenic environment in peripheral tissues. Through the screening of gene differentially expressed, we also identified two DC-10-specific markers, CD141 and CD163 that in combination with CD14 and CD16 allow their identification and isolation in vivo. CD141+CD163+CD14+CD16+ cells isolated from peripheral blood of healthy donors produce IL-10 at steady state and upon activation, in the absence of IL-12, and prime allogeneic naïve CD4+ T cells. Furthermore, preliminary results indicate that allogeneic naïve CD4+ T cells primed with ex vivo isolated DC-10 produce IL-10 when re-stimulated with the same allo-antigen. To achieve the second aim, we studied the ability of DC-10 to modulate allogeneic CD8+ T cells. DC-10 activate allogeneic CD8+ T cells at lower levels compared to mDC, as demonstrated by the expression of activation markers and IFN-γ production. Despite the expression of HLA class I and co-stimulatory molecules, DC-10 poorly stimulate the proliferation of allogeneic CD8+ T cells, which is partially rescued by the addition of exogenous IL-12. Moreover, DC-10 inhibit mDC-induced proliferation of allogeneic CD8+ T cells in a dose-dependent manner, suggesting an active mechanism of suppression mediated by DC-10. This immunomodulatory effect is contact-independent, as shown by transwell experiments. In parallel, we assessed the ability of DC-10 to prime allogeneic T cells in vivo in NSG mice co-injected with DC-10 and allogeneic PBMC. Upon in vitro re-stimulation of spleen cells with allo-antigens, CD4+ and CD8+ T cells from mice injected with DC-10 proliferate less compared to T cells isolated from control mice injected with mDC. Conversely, response to 3rd party allo-antigens is comparable. These data indicate that DC-10 prime T cells in vivo and induce anergic allo-antigen specific T cells. In conclusion, we identify the biomarkers of DC-10 that allow their study in vivo in healthy and pathological conditions. Moreover, we demonstrate the ability of DC-10 to modulate allogeneic CD8+ T cell responses, supporting the use of DC-10 as DC-based therapy in transplantation. DC-10 may indeed promote tolerance via allo-specific CD4+ Tr1 cells, and, concomitantly, limit allo-reactive CD8+ T cell responses.
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Teaster, Neal D. Chapman Kent Dean. "A regulatory role for N-acylethanolamine metabolism in Arabidopsis thaliana seeds and seedlings." [Denton, Tex.] : University of North Texas, 2009. http://digital.library.unt.edu/permalink/meta-dc-10978.

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ZeRuth, Gary T. "Isolation and Functional Characterization of a Dioxin-Inducible CYP1A Regulatory Region From Zebrafish (Danio rerio)." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002447.

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Ruzek, Mitch James. "Evolution of a conserved gene regulatory network among echinoderms : a comparison of genes expressed in the skeletogenetic lineage of the ophuroid Ophiocoma wendtii and the echinoid Strongylocentrotus purpuratus." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0003181.

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Jackson, Erin M. "Integrating Leader-Member Exchange and Organizational Justice: Why Justice Depends on Relationship Quality." [Tampa, Fla] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002366.

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Blumenthal, Pamela M. "Local Land Use Regulatory Regimes and Residential Development Outcomes| An Analysis of Subdivision Review in Four Counties in the DC Region." Thesis, The George Washington University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3598490.

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Land use regulations affect housing prices, with more restrictive regulatory environments associated with higher prices. Yet, regulations are only a part of the regulatory regime in which land use decisions are made, leading to the question: how do land use regulatory regimes affect housing prices? This study examines and compares the land use regulatory regimes of four counties, Frederick, MD, Montgomery, MD, Fairfax, VA, and Loudoun, VA through interviews, project files, and regulatory review to learn how the combination of structures, rules, norms, principles, and expectations, relate to housing prices. State differences in the tools available lead to Virginia counties having a more predictable, but not faster, subdivision review process than Maryland counties. More importantly, local differences in developer contributions for mitigating the impact of development, community involvement, and perspectives on development affect the cost and predictability of the residential development review process. These jurisdictional differences support the need to focus research on regulatory regimes rather than simply regulations to identify changes to reduce unnecessary costs that increase house prices.

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Karnam, Anupama. "Role of Wnt/β-catenin pathway in the anti-inflammatory mechanism of therapeutic normal immunoglobulins Wuchereria bancrofti filaria activates human dendritic cells and polarizes T helper 1 and regulatory T cells via toll-like receptor 4 Regulatory T cells induce activation rather than suppression of human basophils." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS642.

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Les immunoglobulines polyclonales intraveineuses (IVIG) sont préparées à partir de plasmas provenant de plusieurs milliers de donneurs sains et utilisées comme traitement dans de nombreuses maladies inflammatoires et autoimmunes. Lors de ma thèse, j’ai investigué si cette thérapie pouvait interférer avec la détection sérique du virus Zika chez des patients atteints du syndrome de Guillain-Barré (GBS). J’ai démontré que la thérapie par IVIG n’interférait pas avec la détection sérique du virus dans le plasma des patients atteints de GBS suivant un traitement aux IVIG. Contrairement aux souris, les IVIG peuvent activer les basophiles humains par une voie différente que celle de l’IL-33. Les IVIG induisent la sécrétion d’Il-4, IL-6 et IL-8 par interaction directe avec les IgE à la surface des basophiles. Cette fonction est dépendante de la fraction F(ab’)2 et implique l’activation de Syk. Ces résultats montrent un nouveau mécanisme dans l’activation des basophiles humains par les IVIG. La dernière partie de ma thèse m’a permis d’étudier le rôle de la voie de signalisation β-caténine sur les effets anti-inflammatoires médiées pars les IVIG. La β-caténine, composante de la voie Wnt, joue un rôle important dans la tolérogénicité des cellules dendritiques (DC) et dans la protection contre l’encéphalomyélite auto-immune expérimentale (EAE). Les données générées montrent que les IVIG activent la voie β-caténine chez les DC humains en plus de la production de Wnt 5a nécessitant une IgG complète ainsi que les co-récepteurs LRP5/6. En dépit de l’induction de β-caténine par les IVIG, cette voie est dispensable pour ses actions anti-inflammatoires in vitro et in vivo dans le modèle EAE
Intravenous immunoglobulin (IVIG) is a therapeutic preparation of pooled normal IgG obtained from the several thousand healthy donors. It is established as first-line therapy for many autoimmune and inflammatory diseases. In the first part of my thesis, I have investigated if IVIG therapy interferes with the serological detection of Zika virus infection in Guillain–Barré syndrome (GBS) patients. By analyzing the plasma of GBS patients treated with IVIG for anti-Zika IgG, I have demonstrated that IVIG therapy in GBS patients does not interfere with the serological Zika detection. The second part addresses the immunoregulatory role of IVIG on human basophil function. Unlike in mice, IVIG does not require DC-SIGN-dependent IL-33 for the activation of human basophils. IVIG directly induces the activation of IL-3-primed human basophils and secretion of IL-4, IL-6, and IL-8 by directly interacting with the basophil surface-bound IgE. This function was F(ab’)2-dependent and involves Syk activation. These results demonstrate a novel mechanism of human basophil activation by IVIG. The last part unravels the signaling pathways associated with IVIG-mediated anti-inflammatory effects specifically the Wnt/β-catenin pathway, which imparts tolerogenic properties to dendritic cells (DCs) and protection against experimental autoimmune encephalomyelitis (EAE). My data shows that IVIG activates β-catenin in human DC along with upregulation of Wnt 5a. Activation of β-catenin requires intact IgG and LRP5/6 co-receptors. However, despite the activation of β-catenin by IVIG, this pathway is dispensable for its anti-inflammatory actions both in vitro and in vivo in the EAE model
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Nghe, Brandon K. "Cascaded Linear Regulator with Positive Voltage Tracking Switching Regulator." DigitalCommons@CalPoly, 2020. https://digitalcommons.calpoly.edu/theses/2173.

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This thesis presents the design, simulation, and hardware implementation of a proposed method for improving efficiency of voltage regulator. Typically, voltage regulator used for noise-sensitive and low-power applications involves the use of a linear regulator due to its high power-supply rejection ratio properties. However, the efficiency of a linear regulator depends heavily on the difference between its input voltage and output voltage. A larger voltage difference across the linear regulator results in higher losses. Therefore, reducing the voltage difference is the key in increasing regulator’s efficiency. In this thesis, a pre switching regulator stage with positive voltage tracking cascaded to a linear regulator is proposed to provide an input voltage to a linear regulator that is slightly above the output of the linear regulator. The tracking capability is needed to provide the flexibility in having different positive output voltage levels while maintaining high overall regulator’s efficiency. Results from simulation and hardware implementation of the proposed system showed efficiency improvement of up to 23% in cases where an adjustable output voltage is necessary. Load regulation performance of the proposed method was also overall better compared to the case without the output voltage tracking method.
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Ge, Ting. "Resonant Cross-Commutated Dc-Dc Regulators with Omni-Coupled Inductors." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/84936.

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The switching noise in a hard-switched point-of-load (POL) converter may result in false turn on, electromagnetic interference issues, or even device breakdown. A resonant cross-commutated buck (rccBuck) converter operates with low noise since all MOSFETs are turned on with zero voltage within a wide load range. A state-space model was developed to calculate the voltage gain, voltage stresses, and current stresses. Design guidelines for the rccBuck converter operating at continuous voltage mode or discontinuous voltage mode are provided. The design methodology of a one-turn inductor with significant ac and dc fluxes is given. Four fabricated one-turn inductors achieved 2.1% higher efficiency and 50% smaller total magnetic volume than the commercial inductors in the same rccBuck converter. The Omni-coupled inductors (OCI), composed of a twisted E-E core and PCB windings, further improve power density and efficiency. The core loss and inductances were modeled from a complex reluctance network. According to the loss-volume Pareto fronts, the total inductor loss was minimized within a smaller volume than that of discrete inductors. The expectations were validated by an OCI-based rccBuck converter switched at 2 MHz with 12 V input, 3.3 V at 20 A output, and peak efficiency of 96.2%. The small-signal model with a good accuracy up to half switching frequency was developed based on the averaged equivalent circuit. The transient performance of an rccBuck regulator is comparable to that of a second-order buck regulator with the same switching frequency, output capacitance, and closed-loop bandwidth.
Ph. D.
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Bevrani, Hassan. "Modeling, Nonlinear and Robust control of DC-DC Switching Regulators." Thesis, K. N. Toosi University of Technology, 1997.

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It is generally known that DC-DC switching regulators are highly nonlinear systems which are subjected to significant variation in the line voltage and load, uncertainty in the circuit parameters and perturbations in switching times. To assure stable operation and acceptable performance despite the disturbances and inevitable uncertainty associated with such systems, highly accurate regulation schemes must be devised. Indeed the routine application of most classical compensation techniques are severely limited when tight regulation measures have to be achieved. These considerations in conjunction with increasing demand for high quality DC-DC switching regulators has necessitated more systematic and precise methodologies in modeling and control design for such systems. The first step in the present thesis is to introduce various techniques for modeling switching regulators specifically models which account for parametric uncertainty and the nonlinear switching effects are intended. Using the models obtained in this fashion, the next step will be to apply nonlinear (input-output feedback linearization) and robust control (Mu-synthesis, Hinf and Kharitonov theorems) techniques to obtain controllers which guarantee satisfactory operation of the system under realistic operating conditions. The resulting controllers are shown to minimize the effect of disturbances and achieve acceptable regulation. The potential superiorities of these methods over classical methodologies are also discussed. At least, two approaches based on Mu-analysis and Kharitonov’s theorem are proposed for the analysis of switching regulators. Applications to practical circuits with buck and cuk converters are illustrated as case studies.
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Books on the topic "Regulatory DC"

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NRC, Regulatory Information Conference (1989 Washington D. C. ). Proceedings of the U.S. Nuclear Regulatory Commission NRC Regulatory Information Conference: Held at the Mayflower Hotel, Washington, DC, April 18-20, 1989. Washington, DC: The Commission, 1989.

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NRC Regulatory Information Conference (1989 Washington, D.C.). Proceedings of the U.S. Nuclear Regulatory Commission NRC Regulatory Information Conference: Held at the Mayflower Hotel, Washington, DC, April 18-20, 1989. Washington, DC: The Commission, 1989.

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NRC Regulatory Information Conference (1989 Washington, D.C.). Proceedings of the U.S. Nuclear Regulatory Commission NRC Regulatory Information Conference: Held at the Mayflower Hotel, Washington, DC, April 18-20, 1989. Washington, DC: The Commission, 1989.

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NRC Regulatory Information Conference (1989 Washington, D.C.). Proceedings of the U.S. Nuclear Regulatory Commission NRC Regulatory Information Conference: Held at the Mayflower Hotel, Washington, DC, April 18-20, 1989. Washington, DC: The Commission, 1989.

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NRC Regulatory Information Conference (1989 Washington, D.C.). Proceedings of the U.S. Nuclear Regulatory Commission NRC Regulatory Information Conference: Held at the Mayflower Hotel, Washington, DC, April 18-20, 1989. Washington, DC: The Commission, 1989.

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Environment, United States Congress House Committee on Interior and Insular Affairs Subcommittee on Energy and the. Nuclear Regulatory Commission reorganization legislation: Hearing before the Subcommittee on Energy and the Environment of the Committee on Interior and Insular Affairs, House of Representatives, One Hundredth Congress, second session, on H.R. 2126 ... H.R. 3049 ... H.R. 3124 ... H.R. 3285 ... H.R. 4134 ... H.R. 4140 ... hearing held in Washington, DC, April 26, 1988. Washington: U.S. G.P.O., 1989.

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United States. Congress. House. Committee on Small Business. The Regulatory Flexibility Act: Hearing before the Committee on Small Business, House of Representatives, One Hundred Third Congress, first session, Washington, DC, July 28, 1993. Washington: U.S. G.P.O., 1993.

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United States. Congress. House. Committee on Small Business. The Regulatory Flexibility Act: Hearing before the Committee on Small Business, House of Representatives, One Hundred Third Congress, first session, Washington, DC, July 28, 1993. Washington: U.S. G.P.O., 1993.

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United States. Congress. House. Committee on Interior and Insular Affairs. Subcommittee on General Oversight and Investigations. Relationship of the Nuclear Regulatory Commission to the nuclear industry: Oversight hearing before the Subcommittee on General Oversightand Investigations of the Committee on Interior and Insular Affairs, House of Representatives, One Hundredth Congress, first session ... hearing held in Washington, DC, June 11, 1987. Washington: U.S. G.P.O., 1988.

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Mitchell, Daniel M. DC-DC switching regulator analysis. New York: McGraw-Hill, 1988.

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Book chapters on the topic "Regulatory DC"

1

Wu, Keng C. "Series Regulator." In Pulse Width Modulated DC-DC Converters, 84–96. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6021-0_7.

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Kislovski, André S., Richard Redl, and Nathan O. Sokal. "Feedforward in Switching Regulators." In Dynamic Analysis of Switching-Mode DC/DC Converters, 265–97. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-7849-5_11.

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Kislovski, André S., Richard Redl, and Nathan O. Sokal. "Free-Running Hysteretic Regulator." In Dynamic Analysis of Switching-Mode DC/DC Converters, 231–42. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-7849-5_9.

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Kislovski, André S., Richard Redl, and Nathan O. Sokal. "Parallel Operation of Switching Regulators." In Dynamic Analysis of Switching-Mode DC/DC Converters, 299–314. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-7849-5_12.

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Bendriss-Vermare, N., N. Gourdin, N. Vey, J. Faget, V. Sisirak, I. Labidi-Galy, I. Le Mercier, et al. "Plasmacytoid DC/Regulatory T Cell Interactions at the Center of an Immunosuppressive Network in Breast and Ovarian Tumors." In Oncoimmunology, 143–61. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-62431-0_8.

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Severns, Rudolf P., and Gordon Ed Bloom. "Small-Signal Models of Complex Converters and Regulators." In Modern DC-to-DC Switchmode Power Converter Circuits, 231–53. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-011-8085-6_10.

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Kislovski, André S., Richard Redl, and Nathan O. Sokal. "General Small-Signal, Low-Frequency Analysis of Switching Regulators." In Dynamic Analysis of Switching-Mode DC/DC Converters, 71–82. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-7849-5_3.

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Kislovski, André S., Richard Redl, and Nathan O. Sokal. "Interconnection of a Power Source and a Switching Regulator." In Dynamic Analysis of Switching-Mode DC/DC Converters, 245–63. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-7849-5_10.

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Multhoff, G., E. A. Repasky, and Peter Vaupel. "Mild Hyperthermia Induced by Water-Filtered Infrared A Irradiation: A Potent Strategy to Foster Immune Recognition and Anti-Tumor Immune Responses in Superficial Cancers?" In Water-filtered Infrared A (wIRA) Irradiation, 129–39. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_10.

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AbstractApart from a number of positive “physiological” effects such as an increase in local blood flow which results in an improved oxygen supply and a reversal of tumor hypoxia, a key hallmark of cancer growth which greatly impairs anti-tumor immune responses, hyperthermia (HT) also exerts beneficial effects on anti-cancer immunity. The water-filtered infrared A (wIRA) irradiation technique achieves tissue temperatures in the fever-range (tT = 39–41 °C) or mild hyperthermia levels (tT = 39–43 °C) up to tissue depths of ≈25 mm in tissues. At tissue temperatures of 39–43 °C, by fostering the reactivity of the “immunological” TME [e.g., the activity of CD8+ cytotoxic T cells, CD4+ helper T cells, dendritic cells (DC), M1 macrophages, natural killer (NK) cells, and NK-like T (NK-T) cells], while compromising immunosuppressive cells [e.g., tumor-associated M2 macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), regulatory T (Treg) cells]. Moreover, elevated temperatures resulting in mild hyperthermia induce the synthesis and release of heat-shock proteins (HSPs), and thereby augment tumor antigenicity.
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Saealal, M. S., A. T. Ramachandran, M. F. Abas, and N. Md Saad. "Synchronize Speed Control for Multiple DC Motors Using Linear Quadratic Regulator." In Proceedings of the International Conference on Computing, Mathematics and Statistics (iCMS 2015), 85–92. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-2772-7_9.

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Conference papers on the topic "Regulatory DC"

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Gartlgruber, Moritz, Daniel Dreidax, Daria Doncevic, Sebastian Steinhauser, Stefan Gröschel, Kai Oliver Henrich, Young-Gyu Park, Carl Herrmann, and Frank Westermann. "Abstract LB-083: Core transcriptional regulatory circuitries in neuroblastoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-083.

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Hegde, Upendra P., and Nitya G. Chakraborty. "Abstract 3722:In vitroinduced regulatory T cells for understanding the nature of peripherally induced regulatory cells in relation to cell mediated immunotherapy for cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3722.

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Saini, Sharanjot, Shahana Majid, Guoren Deng, Soichiro Yamamura, Koji Ueno, Yi Chen, Saif Zaman, and Rajvir Dahiya. "Abstract 2033: Regulatory role of miR-203 in prostate cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2033.

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Pochi, Subbarayan R., Nikesh Doshi, Xiaoqing Han, Zhiqiang Wang, Anthony Capobianco, David Robbins, and Bach Ardalan. "Abstract 4019: Regulatory role of Gli motifs in thymidylate synthase expression ." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4019.

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Dingar, Dharmendra, Amanda R. Wasylishen, Michelle Chan-Seng-Yue, Ling Huang, Christina Bros, William Tu, Natalie Meyer, Paul C. Boutros, and Linda Z. Penn. "Abstract LB-117: Myc phosphorylation suppresses transformation through novel regulatory regions." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-117.

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Rollison, Dana E., Shalaka S. Hampras, Jane L. Messina, Neil A. Fenske, Basil S. Cherpelis, Michael J. Schell, Rhianna Reed, et al. "Abstract 4960: Recent ultraviolet radiation exposure and circulating immunosuppressive T-regulatory cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4960.

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Liu, Yu, Michael Edmonson, Xiaotu Ma, Michael Rusch, Yongjin Li, Benshang Li, Shuhong Shen, A. Thomas Look, and Jinghui Zhang. "Abstract 1574: Computational approach for discovery of regulatory noncoding variants in cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1574.

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Corona, Rosario I., Emily Adler, Janet M. Lee, Norma Rodriguez-Malave, Paulette Mhawech-Fauceglia, Heidi Sowter, Dennis J. Hazelett, Kate Lawrenson, and Simon A. Gather. "Abstract 2418: Characterization of the PAX8 regulatory network in epithelial ovarian cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2418.

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Hilmarsdottir, Bylgja, Skarphedinn Halldorsson, Maria T. Grinde, Anna Barkovskaya, Solveig Pettersen, Thorarinn Gudjonsson, Siver A. Moestue, Ottar Rolfsson, and Gunhild M. Mælandsmo. "Abstract 4412: Metabolic reprogramming in EMT - targeting regulatory nodes in mesenchymal cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4412.

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Kiely, Patrick A., George Baillie, Miles Houslay, and Rosemary O'Connor. "Abstract 3955: Identification of RACK1 as a novel regulatory subunit of PP2A." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3955.

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Reports on the topic "Regulatory DC"

1

Drive modelling and performance estimation of IPM motor using SVPWM and Six-step Control Strategy. SAE International, April 2021. http://dx.doi.org/10.4271/2021-01-0775.

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This paper presents a comprehensive evaluation of the performance of an interior permanent magnet (IPM) traction motor drive, and analyses the impact of different modulation techniques. The most widely used modulation methods in traction motor drives are Space vector modulation (SVPWM), over-modulation, and six-step modulation have been implemented. A two-dimensional electromagnetic finite element model of the motor is co-simulated with a dynamic model of a field-oriented control (FOC) circuit. For accurate tuning of the current controllers, extended complex vector synchronous frame current regulators are employed. The DC-link voltage utilization, harmonics in the output waveforms, torque ripple, iron losses, and AC copper losses are calculated and compared with sinusoidal excitation. Overall, it is concluded that the selection of modulation technique is related to the operating condition and motor speed, and a smooth transition between different modulation techniques is essential to achieve a better performance.
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