Relevant bibliographies by topics / Plasmacytoïde dendritic cells

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  2. Dissertations / Theses
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Academic literature on the topic 'Plasmacytoïde dendritic cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Plasmacytoïde dendritic cells"

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Jegalian, Armin G., Fabio Facchetti, and Elaine S. Jaffe. "Plasmacytoid Dendritic Cells." Advances in Anatomic Pathology 16, no. 6 (2009): 392–404. http://dx.doi.org/10.1097/pap.0b013e3181bb6bc2.

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Waller, Edmund K. "Mobilizing plasmacytoid dendritic cells." Blood 129, no. 19 (2017): 2600–2602. http://dx.doi.org/10.1182/blood-2017-03-774703.

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Maroso, Mattia. "Depleting plasmacytoid dendritic cells." Science 372, no. 6545 (2021): 929.17–929. http://dx.doi.org/10.1126/science.372.6545.929-q.

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Smit, Joost J., Brian D. Rudd, and Nicholas W. Lukacs. "Plasmacytoid dendritic cells inhibit pulmonary immunopathology and promote clearance of respiratory syncytial virus." Journal of Experimental Medicine 203, no. 5 (2006): 1153–59. http://dx.doi.org/10.1084/jem.20052359.

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Respiratory syncytial virus (RSV) infection is widely spread and is a major cause of bronchiolitis in infants and high-risk adults, often leading to hospitalization. RSV infection leads to obstruction and inflammation of the airways and induction of innate and acquired immune responses. Because dendritic cells (DCs) are essential in the elicitation of these immune responses, we investigated the presence and the role of dendritic cell subtypes upon RSV infection in the lung. Here, we report that RSV infection increased the number of both conventional and plasmacytoid dendritic cells in the lung and the lung-draining lymph nodes. In particular, the increase in plasmacytoid dendritic cell numbers was sustained and lasted until 30 d after infection. Depletion of plasmacytoid dendritic cells resulted in decreased RSV clearance. In addition, depletion of plasmacytoid dendritic cells resulted in an exacerbation of all manifestations of immune-mediated pathology caused by RSV infection. In conclusion, this study demonstrates that both conventional and plasmacytoid dendritic cells are attracted to the site of RSV infection. It is demonstrated that plasmacytoid dendritic cells play a protective role during RSV infection by modulation of local immune responses.
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Weslow-Schmidt, Janet L., Nancy A. Jewell, Sara E. Mertz, J. Pedro Simas, Joan E. Durbin, and Emilio Flaño. "Type I Interferon Inhibition and Dendritic Cell Activation during Gammaherpesvirus Respiratory Infection." Journal of Virology 81, no. 18 (2007): 9778–89. http://dx.doi.org/10.1128/jvi.00360-07.

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ABSTRACT The respiratory tract is a major mucosal site for microorganism entry into the body, and type I interferon (IFN) and dendritic cells constitute a first line of defense against viral infections. We have analyzed the interaction between a model DNA virus, plasmacytoid dendritic cells, and type I IFN during lung infection of mice. Our data show that murine gammaherpesvirus 68 (γHV68) inhibits type I IFN secretion by dendritic cells and that plasmacytoid dendritic cells are necessary for conventional dendritic cell maturation in response to γHV68. Following γHV68 intranasal inoculation, the local and systemic IFN-α/β response is below detectable levels, and plasmacytoid dendritic cells are activated and recruited into the lung with a tissue distribution that differs from that of conventional dendritic cells. Our results suggest that plasmacytoid dendritic cells and type I IFN have important but independent roles during the early response to a respiratory γHV68 infection. γHV68 infection inhibits type I IFN production by dendritic cells and is a poor inducer of IFN-α/β in vivo, which may serve as an immune evasion strategy.
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Bardawil, Tara, Samar Khalil, Mazen Kurban, and Ossama Abbas. "Diagnostic utility of plasmacytoid dendritic cells in dermatopathology." Indian Journal of Dermatology, Venereology and Leprology 87 (February 5, 2021): 3–13. http://dx.doi.org/10.25259/ijdvl_638_19.

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Differentiating cutaneous diseases that mimic each other clinically and histopathologically can at times be a challenging task for the dermatopathologist. At the same time, differentiation of entities with overlapping features may be crucial for patient management. Although not seen in normal skin, plasmacytoid dendritic cells usually infiltrate the skin in several infectious, inflammatory/autoimmune and neoplastic entities. Plasmacytoid dendritic cells can be identified in tissue using specific markers such as CD123 and/or blood-derived dendritic cell antigen-2. Plasmacytoid dendritic cells are the most potent producers of type I interferons and their activity may therefore be assessed indirectly in tissue using human myxovirus resistance protein A, a surrogate marker for type I interferon production. In recent years, accumulating evidence has established the utility of evaluating for specific plasmacytoid dendritic cell-related parameters (plasmacytoid dendritic cell content, distribution and clustering and/ or human myxovirus resistance protein A expression) as a diagnostic tool in differentiating cutaneous diseases with overlapping features such as the alopecias, lupus and its mimics, and neoplastic entities. In this review, we provide an update on the current evidence on this topic and on the contexts where this can be a useful adjunct to reach the histopathological diagnosis.
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Tassone, Laura, Daniele Moratto, William Vermi, et al. "Defect of plasmacytoid dendritic cells in warts, hypogammaglobulinemia, infections, myelokathexis (WHIM) syndrome patients." Blood 116, no. 23 (2010): 4870–73. http://dx.doi.org/10.1182/blood-2010-03-272096.

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Abstract Warts, hypogammaglobulinemia, infections, myelokathexis (WHIM) syndrome is a genetic disease that is caused by heterozygous mutations of the CXCR4 gene. These mutations confer an increased leukocyte response to the CXCR4-ligand CXCL12, resulting in abnormal homeostasis of many leukocyte types, including neutrophils and lymphocytes. Analysis of the myeloid and plasmacytoid dendritic cell blood counts in WHIM patients revealed a striking defect in the number of plasmacytoid dendritic cells as well as a partial reduction of the number of myeloid dendritic cells, compared with healthy subjects. Moreover, the production of interferon-α by mononuclear cells in response to herpes simplex infection, or after stimulation with the Toll-like receptor 9 ligand CpG, was undetectable in WHIM patients. Because plasmacytoid dendritic cells play a key role in the defense against viruses and their generation and motility are in part dependent on CXCR4, we hypothesized that the susceptibility of WHIM patients to warts is related to the abnormal homeostasis of plasmacytoid dendritic cells.
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Fuchsberger, Martina, Hubertus Hochrein, and Meredith O'Keeffe. "Activation of plasmacytoid dendritic cells." Immunology & Cell Biology 83, no. 5 (2005): 571–77. http://dx.doi.org/10.1111/j.1440-1711.2005.01392.x.

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Colonna, Marco, Giorgio Trinchieri, and Yong-Jun Liu. "Plasmacytoid dendritic cells in immunity." Nature Immunology 5, no. 12 (2004): 1219–26. http://dx.doi.org/10.1038/ni1141.

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Biessen, Erik A. L., and Anette Christ. "Plasmacytoid Dendritic Cells in Atherosclerosis." Circulation 130, no. 16 (2014): 1340–42. http://dx.doi.org/10.1161/circulationaha.114.012641.

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Dissertations / Theses on the topic "Plasmacytoïde dendritic cells"

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Assil, Sonia. "Mechanism of viral immunostimulatory signal transmission from infected cells to plasmacytoid dendritic cells." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSEN069.

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Les cellules dendritiques plasmacytoides (pDCs), spécialisées dans la réponse antivirale, produisent de fortes quantités d’interféron (IFN) lorsqu’elles sont en contact avec des cellules infectées par des virus. Pourtant, les pDCs sont réfractaires à l’infection. Ce mécanisme d’activation de la réponse antivirale par le contact physique avec les cellules infectées, nouvellement découvert, constituerait un aspect général des voies de défense de l’hôte contre les virus.En utilisant le virus de l’Hépatite C et de la Dengue comme modèle viral, nous avons observé une réorganisation moléculaire au niveau des contacts entre les pDCs et les cellules infectées. La polarisation d’éléments cellulaires, notamment de régulateurs du cytosquelette d’actine et de molécules de la machinerie d’endocytose en direction du contact favoriserait son établissement et/ou sa stabilisation ainsi qu’une transmission efficace d’éléments viraux, ensuite reconnus par les pDCs. Nous avons également démontré que les pDCs effectuent des contacts plus stables et présentent une polarisation plus importante d’éléments cellulaires aux contacts avec des cellules infectées qu’avec des cellules non infectées. Ces interactions présentent des similarités avec les synapses, contacts cellulaires organisés impliqués dans la communication cellulaire. Notamment, les synapses immunologiques jouent un rôle important dans l’activation de la réponse immunitaire adaptative. Nous proposons donc de nommer ces contacts activateurs de pDCs des « synapses immunologiques innées ». Ce mécanisme représenterait un processus de reconnaissance des infections par les pDCs généralisable à différents types de virus, par « scan » du statut infectieux des cellules par contact. Nos résultats suggèrent également que des éléments viraux s’accumulent au niveau de ces contacts. Ces éléments diffèrent en fonction du type d’infection. Notamment, nous avons mis en évidence dans un contexte d’infection par le virus de la Dengue que des structures virales non canoniques et non infectieuses, différentes des particules virales infectieuses dites « classiques », jouent un rôle important dans l’activation de la réponse antivirale. Notre travail apporte un nouvel angle d’analyse de l’activation des pDCs et des stratégies de détection des infections virales par l’hôte<br>Plasmacytoid dendritic cells (pDCs), specialized in the antiviral response, are important producers of interferons (IFN) after cell-cell contacts with virally infected cells. Nonetheless, they are poorly permissive to the majority of viral infections. This newly uncovered mechanism of the activation of an antiviral response by physical cell-cell contacts with infected cells could constitute a general aspect of the host defense against viral infections.Using Hepatitis C virus and Dengue virus as models, we observed a molecular reorganization of the contacts between pDCs and infected cells. The polarization toward contacts of cellular elements, such as regulators of the actin cytoskeleton and components of the endocytic machinery could favor their establishment and/or their stabilization, as well as the efficient transmission of viral elements that are recognized by pDCs. We also demonstrated that pDCs contacts with infected cells are more stable and present a higher polarization of cellular components than contacts with uninfected cells. These interactions present similarities with synapses, a type of organized contact involved in cell-to-cell communication. Notably, immunological synapses are known to play an important role in the activation of the adaptive immune response. We thus propose to call these pDC-activating contacts « innate immunological synapses ». This mechanism could represent a general process of recognition of viral infections by pDCs, by « scanning » the infectious status of the cells by cell-cell contacts. Our results also suggest that viral elements cluster at the level of contacts. These elements differ depending on the type of viral infection. Notably, we observed in the context of Dengue virus infection that non-infectious non-canonical viral structures, that differ from the « classical » viral infectious particles, play an important role in the activation of the antiviral response. Our work brings a new light in the mechanisms of pDC activation and in the host defense strategies against viral infection
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Ceroi, Adam. "Les "Liver X Receptors" : modulateurs des fonctions des cellules dendritiques plasmocytoïdes et leur contrepartie leucémique." Thesis, Besançon, 2015. http://www.theses.fr/2015BESA3015/document.

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Chaque cadre doit contenir un résumé de 1700 caractères maximum, espaces compris. En cas de dépassement, la coupure sera automatique. Le doctorant adresse son texte sous forme électronique selon les recommandations de la bibliothèqueLes "Liver X receptors " (LXR) sont des récepteurs nucléaires impliqués dans Phoméostasie du cholestérol. Dans les macrophages, la stimulation de la voie LXR accroît la clairance des corps apoptotiques et réprime la réponse inflammatoire. Les LXR inhibent également la prolifération et la survie de cellules malignes.L'activation des LXR dans les cellules dendritiques plasmocytoïdes (PDG) augmentent la clairance des microparticules (MP), via l'induction du récepteur au phosphatidylsérines BAIL L'internalisation des MP active la voie NF-KB ou la voie LXR pour des MP dérivées respectivement, de cellules endothéliales (EMP) ou plaquettaires (PMP). Ces deux voies de signalisation se réprimaient mutuellement, déterminant la réponse inflammatoire des PDG.La contrepartie leucémique des PDC (LPDC) est à l'origine d'une leucémie aiguë agressive, la BPDCN. Nous avons observé une dérégulation de Phoméostasie du cholestérol dans ces cellules. L'activation de la voie LXR entraine un efflux du cholestérol associé à un effet cytotoxique et antiprolifératif. Ils peuvent impliquer : la répression de NF-KB ; ainsi que l'inhibition de la signalisation induite par le facteur de survie IL-3 (incluant STAT5 et Akt). L'utilisation d'un modèle xénogénique murin de BPDCN traitée par agoniste LXR montre une diminution de la cytopénie induite par les LPDC et des infiltrats spléniques et médullaires.Ces travaux démontrent la fonctionnalité de la voie LXR dans les PDC et LPDC, ainsi qu'une régulation croisée avec NF-KB. L'activation de cette voie a démontré son implication dans la clairance des MP et la régulation de la réponse inflammatoire des PDC, ainsi qu'un effet anti-leucémique sur les LPDC<br>Nuclear Liver X Receptors (LXR) are involved in cholesterol homeostasis. In macrophages, LXR promote apoptotic body/cell clearance and repress inflammatory responses. LXR are also shown to inhibit proliferation and survival of malignant cells.In plasmacytoid dendritic cells (PDC), LXR stimulation increases microparticle (MP) engulfment via the increased expression of the PS receptor, BAIL MP engulfment induced NF-icB or LXR activation, depending on the endothelial (EMP) or platelet (PMP) origin of MP, respectively. Overall, we show a crosstalk involving LXR and NF-KB, which dictates the inflammatory fate of PDC engulfing MP.The leukemic PDC counterpart (LPDC) is responsible of an aggressive hematologic malignancy, called blastic plasmacytoid dendritic cell neoplasm (BPDCN). In contrast to healthy PDC and other acute leukemias (including lymphoid and myeloid acute leukemias), we report here a specific downregulation of cholesterol homeostasis-related genes in LPDC. LXR pathway activation increases cholesterol efflux and inhibits cell proliferation and survival. This may involve: inhibition of NF-KB signaling pathway and of signaling pathways induced by the survival factor IL-3 (involving Akt and STAT5). Using a xenogeneic mouse model of BPDCN, LXR agonist treatment reduces BPDCN-induced cytopenia as well as bone marrow and spleen LPDC infiltration.Overall, we demonstrate that LXR receptors are functional in PDC and LPDC and are involved in a cross-regulation mechanism with NF-KB. LXR receptors promote MP clearance and control inflammatory responses in PDC, as well as exert an anti-leukemic therapeutic effect in BPDCN via several mechanisms, including cholesterol efflux
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Futsch, Nicolas. "Caractérisation de l’activation des cellules dendritiques plasmacytoïdes par les virus HTLV-1 et HTLV-2 et de son importance dans la symptomatologie viro-induite." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSEN067/document.

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Le virus T-lymphotrope humain de type 1 (HTLV-1) est l’agent étiologique de deux principales pathologies : la leucémie/lymphome à cellules T de l’adulte (ATLL) et la paraparésie spastique tropicale/myélopathie associée à HTLV-1 (HAM/TSP). Ces deux maladies sont caractérisées par des phénotypes immunitaires opposés, puisque l’ATLL est associée à une immunosuppression et l’HAM/TSP à une réponse pro-inflammatoire. Les mécanismes qui déterminent l’évolution de l’infection chronique vers l’une ou l’autre de ces maladies sont peu connus. L’interféron de type 1 (IFN-I) a une fonction ambiguë dans l’organisme. Si cette cytokine contribue à la réponse immunitaire précoce, elle est également associée au développement de pathogenèses pour des infections virales persistantes. Les cellules dendritiques plasmacytoïdes (pDCs) ont la particularité de produire de grandes quantités d’IFN-I après la reconnaissance de cellules infectées par des virus. Nous avons montré que ceci était également vrai pour HTLV-1, puisque le contact entre une cellule infectée par HTLV-1 et la pDC est nécessaire à la production d’IFN-I. Cette production est induite par la particularité de HTLV-1 à s’accumuler en surface des cellules infectées, au sein d’une structure préalablement définie sous le terme de biofilm viral. La nature de la matrice extracellulaire dans laquelle est accumulée le virus régule la réponse IFN-I par les pDCs, la présence de l’antigène Galβ(1-3)GalNAc désialylé à la surface des cellules infectées contribuant à réduire cette réponse IFN-I. Nous avons également observé que des cellules infectées par le virus HTLV-2, virus phylogénétique proche de HTLV-1 mais peu pathogène, tendent à induire une plus faible production d’IFN-I, mais une meilleure maturation des pDCs. Nous avons enfin montré que la fréquence des pDCs dans le sang et leur capacité à répondre à un stimulus est similaire chez des patients HAM/TSP, des porteurs asymptomatiques et des individus sains. Ces résultats contrastent avec des études antérieures qui montrent une diminution de la fréquence des pDCs chez les patients ATLL et une diminution de leur activité chez les individus infectés. Le nombre et la fonction des pDCs pourraient ainsi contribuer à l’orientation de la pathogenèse vers l’ATLL ou l’HAM/TSP<br>HTLV-1 (Human T-lymphotropic virus type 1) is the etiological agent of two main diseases: the adult T-cell leukemia/lymphoma (ATLL) and the HTLV-1 associated myelopathy/tropical spastic paraparesis, which are characterized by different immune phenotypes. While the ATLL is linked to an immunosuppressive state, the HAM/TSP is linked to a pro-inflammatory state in patients. The mechanisms contributing to the development of these two diseases in the HTLV-1 infected individuals are poorly understood. Type I interferon (IFN-I) has ambivalent functions in the organism. While this cytokine is an effector of early immune responses, several studies have reported a negative impact of this cytokine during chronic infections. The plasmacytoid dendritic cells (pDCs) are the main producers of IFN-I in vivo, and can produce high amounts of this cytokine after the recognition of virally infected cells. We have shown that pDCs are able to recognize HTLV-1-infected cells, thus leading to the production of IFN-I. pDCs’ triggering is mediated by the accumulated viral particles at the surface of the infected cells, within a carbohydrate-rich structure, previously described as the viral biofilm. The nature of the extracellular matrix itself seems to regulate IFN-I production by pDCs, since the exposition of an asialylated Galβ(1-3)GalNAc glycan at the surface of the HTLV-infected cells reduces the IFN-I production. We also observed that HTLV-2 (a close relative of HTLV-1)-infected cells, in contrast to HTLV-1-infected cells, tend to induce a lower production of IFN-I after being recognized by the pDCs but a greater maturation of the latter. Finally, we have shown that pDCs’ frequency in the blood and their ability to produce IFN-α after an ex vivo stimulation is equivalent in healthy donors, asymptomatic HTLV-1 carriers and HAM/TSP patients. This result contrasts with previous studies which demonstrated that blood circulating pDCs’ frequency is reduced in ATLL patients and that pDCs from HTLV-1 infected individuals have a reduced ability to produce IFN-α after stimulation. Thus, dysregulation of the frequency and functionality of pDCs could contribute to the development of one disease or the other
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Netravali, Ilka Arun. "Elucidation of plasmacytoid dendritic cell development." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11311.

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Most currently defined hematopoietic progenitor pools are heterogeneous, contributing to uncertainty regarding the development of certain blood cells. The origins of plasmacytoid dendritic cells, for instance, have long been controversial and progenitors exclusively committed to this lineage have never been described. We show here that the fate of hematopoietic progenitors is determined in part by their surface levels of 9-O-acetyl sialic acid. Pro-plasmacytoid dendritic cells were identified as lineage negative 9-O-acetyl sialic acid low progenitors that lack myeloid and lymphoid potential but differentiate into pre-plasmacytoid dendritic cells. The latter cells are also lineage negative, 9-O-acetyl sialic acid low cells but are exclusively committed to the plasmacytoid dendritic cell lineage. Levels of 9-O-acetyl sialic acid provide a distinct way to define progenitors and thus facilitate the study of hematopoietic differentiation.
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Kim, Jong-won. "Signalling initiation by blood dendritic cell antigen 2, a novel immunoglobulin receptor on plasmacytoid dendritic cells." Thesis, Imperial College London, 2018. http://hdl.handle.net/10044/1/63862.

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The focus of this project is a human-specific C-type lectin with potential roles in cell signalling: blood dendritic cell antigen 2 (BDCA-2). BDCA-2, a plasmacytoid dendritic cell-specific molecular marker, has been evaluated as a therapeutic target against auto-immune disorders, because antibodies to BDCA-2 inhibit the production of type I interferon. Accordingly, key goals of the project were to identify endogenous ligands for BDCA-2, to characterise the mechanism of ligand binding and ultimately to determine how ligands stimulate signalling pathways. A combination of BDCA-2 affinity chromatography column and mass spectrometry revealed that α2 macroglobulin and immunoglobulins, IgA, IgM and IgG are potential endogenous ligands in human serum. Competition binding studies conducted to characterise the binding affinity for each glycoprotein demonstrated that IgA has the highest affinity. Strategies for biochemical development of defined glycoforms of IgG Fc domain were established. The Chinese hamster ovary cell system for expression of Fc domain and the activity of enzymes necessary for chemoenzymatic glycoengineering have been tested. BDCA2 organisation in the cell membrane was studied by development of a transfected cell system which was analysed by affinity purification of BDCA-2 followed by analysis of protein-protein interactions. The results demonstrate that it is likely that BDCA-2 assembles with Fc receptor γ-chain in a 2:2 complex.
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Seeds, Rosalind E. "Innate recognition of viruses by plasmacytoid dendritic cells." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491973.

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Plasmacytoid dendritic cells (pDCs) are thought to be specialized for early viral recognition and secrete large amounts of the anti-viral cytokines type I interferon (lFNa/f3). This thesis studied viral recognition by pDCs and aimed to identify novel viral sensing receptors for viral glycoproteins. Murine pDCs were found to express the predominantly myeloid restricted lectins (mannose receptor, SIGNRI, Dectin-I and Dectin-2); a scavenger receptor, immunomodulatory receptor-ligand pairs (CD200R, CD200, SIRPa and CD47) and myeloid differentiation antigens (F4/80 and 7/4). This extends the known phenotype of pDCs and identified candidate receptors for further study. A protocol based on flow cytometric intracellular staining was developed to measure IFNa/f3 production by pDCs. This, together with an IFNa ELISA and IFN bioassay, was used to investigate viral recognition by pDCs. HI and H5 subtypes of influenza virus haemagglutinin (HA) and gp 120 from human immunodeficiency virus (HIVICN54) stimulated IFN production by splenocytes (containing pDCs). Mannan inhibited inactivated influenza virus (A/Guangdong/25/93), HA and gpl20 stimulated IFN production which implied a role for a mannose specific receptor in viral sensing, however, no requirement for mannose receptor or SIGNRI was observed. IFN induction by inactivated influenza virus, HA and gpl20 was also dependent on MyD88, but influenza virus recognition was not dependent on Toll-like receptor (TLR)2 or TLR4, raising the possibility of glycoprotein recognition through another TLR. The ability of CD200 to modulate IFNa induction was also tested. Consistent with the known inhibitory functions of CD200 through CD200R, CD200 knock-out macrophages produced more IFNa in response to the MyD88-independent stimulus polyinosinic-polycytidylic acid. In contrast, the blocking anti-CD200 monoclonal antibody OX90 inhibited MyD88-dependent IFNa production by spleen cells stimulated with influenza virus and CpG ODN suggesting that C0200 could promote IFNa production. C0200 may therefore differentially regulate IFNa induction pathways.
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Kawamura, Kazuko. "Virus-stimulated plasmacytoid dendritic cells induce CD4[+] cytotoxic regulatory T cells." Kyoto University, 2006. http://hdl.handle.net/2433/143873.

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Preston, Stephen. "The recruitment of plasmacytoid dendritic cells in DNA vaccination." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497075.

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Singh, Rena. "Phenotypic and functional characterisation of myeloid and plasmacytoid dendritic cells." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1446340/.

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Cord blood transplantation (CBT) is an alternative to bone marrow transplantation (BMT) and is associated with a reduced severity of graft versus host disease (GvHD). Recipient and donor dendritic cells (DCs) are involved in the development of GvHD, and two main subsets, myeloid DCs (MDCs) and plasmacytoid DCs (PDCs), with different immunological functions, have been identified in adult peripheral blood (APB). In this thesis, the presence, phenotype and functional characteristics of these two DC subsets were investigated in CB. Absolute cell counts, the expression of a number of markers and the endocytic capacities were studied on highly purified MDCs and PDCs by flow cytometry. The cytokine profile of stimulated DC subsets was determined using a multiple cytokine detection system. The allostimulatory capacity was studied in vitro and the cytokine production of the cultures was also assessed. The results showed the presence of MDCs and PDCs in CB, with PDCs as the predominant population. Surface marker expression differed between CB DC subsets, and levels of expression were generally lower compared to APB. Stimulated CB MDCs and PDCs secreted Thl and Th2 cytokines, respectively. CB MDCs had a higher endocytic capacity than PDCs, as shown for APB. The allostimulatory capacity of CB MDCs was higher than CB and APB PDCs, but lower than APB MDCs. Comparisons of fresh and frozen cells revealed a reduced allostimulatory capacity of frozen CB DC subsets, not apparent in APB. There was preferential secretion of Th2 cytokines following allogeneic stimulation with CB MDCs and PDCs. The results showed different phenotypic and functional characteristics of CB MDCs compared to PDCs. The studies confirmed the immature status of CB DCs and their capacity to mount adult level responses when appropriately stimulated. Therefore, these in vitro studies may help to explain the reduced incidence and severity of GvHD following CBT.
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Bandoła, Joanna, Cornelia Richter, Martin Ryser, et al. "Neurotrophin Receptor p75NTR Regulates Immune Function of Plasmacytoid Dendritic Cells." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-230813.

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Plasmacytoid dendritic cells (pDCs) regulate innate and adaptive immunity. Neurotrophins and their receptors control the function of neuronal tissue. In addition, they have been demonstrated to be part of the immune response but little is known about the effector immune cells involved. We report, for the first time, the expression and immune-regulatory function of the low affinity neurotrophin receptor p75 neurotrophin receptor (p75NTR) by the antigen-presenting pDCs, mediated by toll-like receptor (TLR) 9 activation and differential phosphorylation of interferon regulatory factor 3 and 7. The modulation of p75NTR on pDCs significantly influences disease progression of asthma in an ovalbumin-induced mouse model mediated by the TLR9 signaling pathway. p75NTR activation of pDCs from patients with asthma increased allergen-specific T cell proliferation and cytokine secretion in nerve growth factor concentration-dependent manner. Further, p75NTR activation of pDCs delayed the onset of autoimmune diabetes in RIP-CD80GP mice and aggravated graft-versus-host disease in a xenotransplantation model. Thus, p75NTR signaling on pDCs constitutes a new and critical mechanism connecting neurotrophin signaling and immune response regulation with great therapeutic potential for a variety of immune disorders.
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Books on the topic "Plasmacytoïde dendritic cells"

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Lane, Andrew A. Blastic Plasmacytoid Dendritic Cell Neoplasm an Issue of Hematology/Oncology Clinics of North America. Elsevier, 2020.

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van der Vlag, Johan, and Jo H. M. Berden. The patient with systemic lupus erythematosus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.
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Book chapters on the topic "Plasmacytoïde dendritic cells"

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Gehrie, Eric, William Van der Touw, Jonathan S. Bromberg, and Jordi C. Ochando. "Plasmacytoid Dendritic Cells in Tolerance." In Methods in Molecular Biology. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-869-0_9.

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Zimmermann, Arthur. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26587-2_87-1.

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Zimmermann, Arthur. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Tumors and Tumor-Like Lesions of the Hepatobiliary Tract. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26956-6_87.

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Goyal, Amrita, Joi B. Carter, and Lyn McDivitt Duncan. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Atlas of Cutaneous Lymphomas. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17217-0_21.

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Cascio, Michael J., and Robert S. Ohgami. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Molecular Pathology Library. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-62146-3_18.

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Kempf, Werner. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Rare Malignant Skin Tumors. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-2023-5_70.

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Subtil, Antonio. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Diagnosis of Cutaneous Lymphoid Infiltrates. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11654-5_43.

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Hudnall, S. David, Melissa A. Much, and Alexa J. Siddon. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Pocket Guide to Diagnostic Hematopathology. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-10630-0_5.

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Miranda, Roberto N., Joseph D. Khoury, and L. Jeffrey Medeiros. "Blastic Plasmacytoid Dendritic Cell Neoplasm." In Atlas of Lymph Node Pathology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7959-8_82.

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O’Brien, Meagan, Olivier Manches, and Nina Bhardwaj. "Plasmacytoid Dendritic Cells in HIV Infection." In Advances in Experimental Medicine and Biology. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4433-6_3.

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Conference papers on the topic "Plasmacytoïde dendritic cells"

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Cooles, Faye AH, Amy E. Anderson, Dennis W. Lendrem, et al. "01.10 Peripheral blood plasmacytoid dendritic cells in early rheumatoid arthritis." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211048.10.

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Van Pottelberge, Geert R. M., Ken R. Bracke, Sarah Vandenbroeck, et al. "Plasmacytoid Dendritic Cells In Pulmonary Lymphoid Follicles Of Patients With COPD." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3882.

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Zhou, Qiao, Richard Cuthbert, Abdulla Watad, et al. "THU0057 PLASMACYTOID DENDRITIC CELLS IN THE ENTHESIS: PHENOTYPING AND FUNCTION INVESTIGATION." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4845.

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Sapienza, Maria Rosaria, Fabio Fuligni, Maria Antonella Laginestra, et al. "Abstract 1951: miRNA expression profile of Blastic plasmacytoid dendritic cell neoplasm." 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.am2013-1951.

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Palomares, O., C. Benito-Villalvilla, X. Jaumont, P. Pfister, P. Tassinari, and J. López-Abente. "Omalizumab Restores the Capacity of Human Plasmacytoid Dendritic Cells to Induce FOXP3+ Regulatory T Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1068.

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Lewkowich, IP, KM Dienger, AA Sproles, JR Clark, and M. Wills-Karp. "Plasmacytoid Dendritic Cells (DC) Limit Myeloid DC Activation, Promoting Resistance to Experimental Asthma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6087.

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Vey, Nelly, Elena Blanc, Vanja Sisirak, et al. "Abstract 1109: The antimicrobial peptide LL37 activates plasmacytoid dendritic cells in breast cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1109.

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Koucký, Vladimír, Kamila Hladíková, Jan Bouček, and Anna Fialová. "Abstract B91: Plasmacytoid dendritic cells in HPV+ and HPV- head and neck cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-b91.

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Sapienza, Maria Rosaria, Manuela Ferracin, Fabio Fuligni, et al. "Abstract 1805: Integrative analysis of microRNAs in blastic plasmacytoid dendritic cell neoplasm." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1805.

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Sapienza, Maria Rosaria, Manuela Ferracin, Fabio Fuligni, et al. "Abstract 1805: Integrative analysis of microRNAs in blastic plasmacytoid dendritic cell neoplasm." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1805.

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