Relevant bibliographies by topics / Dendritic cell

Academic literature on the topic 'Dendritic cell'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 July 2024

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Journal articles on the topic "Dendritic cell"

Christie, J. M., and G. L. Westbrook. "Regulation of Backpropagating Action Potentials in Mitral Cell Lateral Dendrites by A-Type Potassium Currents." Journal of Neurophysiology 89, no. 5 (May 1, 2003): 2466–72. http://dx.doi.org/10.1152/jn.00997.2002.

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Dendrodendritic synapses, distributed along mitral cell lateral dendrites, provide powerful and extensive inhibition in the olfactory bulb. Activation of inhibition depends on effective penetration of action potentials into dendrites. Although action potentials backpropagate with remarkable fidelity in apical dendrites, this issue is controversial for lateral dendrites. We used paired somatic and dendritic recordings to measure action potentials in proximal dendritic segments (0–200 μm from soma) and action potential-generated calcium transients to monitor activity in distal dendritic segments (200–600 μm from soma). Somatically elicited action potentials were attenuated in proximal lateral dendrites. The attenuation was not due to impaired access resistance in dendrites or to basal synaptic activity. However, a single somatically elicited action potential was sufficient to evoke a calcium transient throughout the lateral dendrite, suggesting that action potentials reach distal dendritic compartments. Block of A-type potassium channels ( I A) with 4-aminopyridine (10 mM) prevented action potential attenuation in direct recordings and significantly increased dendritic calcium transients, particularly in distal dendritic compartments. Our results suggest that I A may regulate inhibition in the olfactory bulb by controlling action potential amplitudes in lateral dendrites.

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Ligon, Cheryl, Eunju Seong, Ethan J. Schroeder, Nicholas W. DeKorver, Li Yuan, Tammy R. Chaudoin, Yu Cai, Shilpa Buch, Stephen J. Bonasera, and Jyothi Arikkath. "δ-Catenin engages the autophagy pathway to sculpt the developing dendritic arbor." Journal of Biological Chemistry 295, no. 32 (June 17, 2020): 10988–1001. http://dx.doi.org/10.1074/jbc.ra120.013058.

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The development of the dendritic arbor in pyramidal neurons is critical for neural circuit function. Here, we uncovered a pathway in which δ-catenin, a component of the cadherin–catenin cell adhesion complex, promotes coordination of growth among individual dendrites and engages the autophagy mechanism to sculpt the developing dendritic arbor. Using a rat primary neuron model, time-lapse imaging, immunohistochemistry, and confocal microscopy, we found that apical and basolateral dendrites are coordinately sculpted during development. Loss or knockdown of δ-catenin uncoupled this coordination, leading to retraction of the apical dendrite without altering basolateral dendrite dynamics. Autophagy is a key cellular pathway that allows degradation of cellular components. We observed that the impairment of the dendritic arbor resulting from δ-catenin knockdown could be reversed by knockdown of autophagy-related 7 (ATG7), a component of the autophagy machinery. We propose that δ-catenin regulates the dendritic arbor by coordinating the dynamics of individual dendrites and that the autophagy mechanism may be leveraged by δ-catenin and other effectors to sculpt the developing dendritic arbor. Our findings have implications for the management of neurological disorders, such as autism and intellectual disability, that are characterized by dendritic aberrations.

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Chen, Wei R., Gongyu Y. Shen, Gordon M. Shepherd, Michael L. Hines, and Jens Midtgaard. "Multiple Modes of Action Potential Initiation and Propagation in Mitral Cell Primary Dendrite." Journal of Neurophysiology 88, no. 5 (November 1, 2002): 2755–64. http://dx.doi.org/10.1152/jn.00057.2002.

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The mitral cell primary dendrite plays an important role in transmitting distal olfactory nerve input from olfactory glomerulus to the soma-axon initial segment. To understand how dendritic active properties are involved in this transmission, we have combined dual soma and dendritic patch recordings with computational modeling to analyze action-potential initiation and propagation in the primary dendrite. In response to depolarizing current injection or distal olfactory nerve input, fast Na+ action potentials were recorded along the entire length of the primary dendritic trunk. With weak-to-moderate olfactory nerve input, an action potential was initiated near the soma and then back-propagated into the primary dendrite. As olfactory nerve input increased, the initiation site suddenly shifted to the distal primary dendrite. Multi-compartmental modeling indicated that this abrupt shift of the spike-initiation site reflected an independent thresholding mechanism in the distal dendrite. When strong olfactory nerve excitation was paired with strong inhibition to the mitral cell basal secondary dendrites, a small fast prepotential was recorded at the soma, which indicated that an action potential was initiated in the distal primary dendrite but failed to propagate to the soma. As the inhibition became weaker, a “double-spike” was often observed at the dendritic recording site, corresponding to a single action potential at the soma. Simulation demonstrated that, in the course of forward propagation of the first dendritic spike, the action potential suddenly jumps from the middle of the dendrite to the axonal spike-initiation site, leaving the proximal part of primary dendrite unexcited by this initial dendritic spike. As Na+conductances in the proximal dendrite are not activated, they become available to support the back-propagation of the evoked somatic action potential to produce the second dendritic spike. In summary, the balance of spatially distributed excitatory and inhibitory inputs can dynamically switch the mitral cell firing among four different modes: axo-somatic initiation with back-propagation, dendritic initiation either with no forward propagation, forward propagation alone, or forward propagation followed by back-propagation.

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Fujishima, Kazuto, Junko Kurisu, Midori Yamada, and Mineko Kengaku. "βIII spectrin controls the planarity of Purkinje cell dendrites by modulating perpendicular axon-dendrite interactions." Development 147, no. 24 (November 24, 2020): dev194530. http://dx.doi.org/10.1242/dev.194530.

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ABSTRACTThe mechanism underlying the geometrical patterning of axon and dendrite wiring remains elusive, despite its crucial importance in the formation of functional neural circuits. The cerebellar Purkinje cell (PC) arborizes a typical planar dendrite, which forms an orthogonal network with granule cell (GC) axons. By using electrospun nanofiber substrates, we reproduce the perpendicular contacts between PC dendrites and GC axons in culture. In the model system, PC dendrites show a preference to grow perpendicularly to aligned GC axons, which presumably contribute to the planar dendrite arborization in vivo. We show that βIII spectrin, a causal protein for spinocerebellar ataxia type 5, is required for the biased growth of dendrites. βIII spectrin deficiency causes actin mislocalization and excessive microtubule invasion in dendritic protrusions, resulting in abnormally oriented branch formation. Furthermore, disease-associated mutations affect the ability of βIII spectrin to control dendrite orientation. These data indicate that βIII spectrin organizes the mouse dendritic cytoskeleton and thereby regulates the oriented growth of dendrites with respect to the afferent axons.

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Kalb, R. G. "Regulation of motor neuron dendrite growth by NMDA receptor activation." Development 120, no. 11 (November 1, 1994): 3063–71. http://dx.doi.org/10.1242/dev.120.11.3063.

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Spinal motor neurons undergo great changes in morphology, electrophysiology and molecular composition during development. Some of this maturation occurs postnatally when limbs are employed for locomotion, suggesting that neuronal activity may influence motor neuron development. To identify features of motor neurons that might be regulated by activity we first examined the structural development of the rat motor neuron cell body and dendritic tree labeled with cholera toxin-conjugated horseradish peroxidase. The motor neuron cell body and dendrites in the radial and rostrocaudal axes grew progressively over the first month of life. In contrast, the growth of the dendritic arbor/cell and number of dendritic branches was biphasic with overabundant growth followed by regression until the adult pattern was achieved. We next examined the influence of neurotransmission on the development of these motor neuron features. We found that antagonism of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor inhibited cell body growth and dendritic branching in early postnatal life but had no effect on the maximal extent of dendrite growth in the radial and rostrocaudal axes. The effects of NMDA receptor antagonism on motor neurons and their dendrites was temporally restricted; all of our anatomic measures of dendrite structure were resistant to NMDA receptor antagonism in adults. These results suggest that the establishment of mature motor neuron dendritic architecture results in part from dendrite growth in response to afferent input during a sensitive period in early postnatal life.

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Nithianandam, Vanitha, and Cheng-Ting Chien. "Actin blobs prefigure dendrite branching sites." Journal of Cell Biology 217, no. 10 (July 24, 2018): 3731–46. http://dx.doi.org/10.1083/jcb.201711136.

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The actin cytoskeleton provides structural stability and adaptability to the cell. Neuronal dendrites frequently undergo morphological changes by emanating, elongating, and withdrawing branches. However, the knowledge about actin dynamics in dendrites during these processes is limited. By performing in vivo imaging of F-actin markers, we found that F-actin was highly dynamic and heterogeneously distributed in dendritic shafts with enrichment at terminal dendrites. A dynamic F-actin population that we named actin blobs propagated bidirectionally at an average velocity of 1 µm/min. Interestingly, these actin blobs stalled at sites where new dendrites would branch out in minutes. Overstabilization of F-actin by the G15S mutant abolished actin blobs and dendrite branching. We identified the F-actin–severing protein Tsr/cofilin as a regulator of dynamic actin blobs and branching activity. Hence, actin blob localization at future branching sites represents a dendrite-branching mechanism to account for highly diversified dendritic morphology.

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Sharp, D. J., W. Yu, and P. W. Baas. "Transport of dendritic microtubules establishes their nonuniform polarity orientation." Journal of Cell Biology 130, no. 1 (July 1, 1995): 93–103. http://dx.doi.org/10.1083/jcb.130.1.93.

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The immature processes that give rise to both axons and dendrites contain microtubules (MTs) that are uniformly oriented with their plus-ends distal to the cell body, and this pattern is preserved in the developing axon. In contrast, developing dendrites gradually acquire nonuniform MT polarity orientation due to the addition of a subpopulation of oppositely oriented MTs (Baas, P. W., M. M. Black, and G. A. Banker. 1989. J. Cell Biol. 109:3085-3094). In theory, these minus-end-distal MTs could be locally nucleated and assembled within the dendrite itself, or could be transported into the dendrite after their nucleation within the cell body. To distinguish between these possibilities, we exposed cultured hippocampal neurons to nanomolar levels of vinblastine after one of the immature processes had developed into the axon but before the others had become dendrites. At these levels, vinblastine acts as a kinetic stabilizer of MTs, inhibiting further assembly while not substantially depolymerizing existing MTs. This treatment did not abolish dendritic differentiation, which occurred in timely fashion over the next two to three days. The resulting dendrites were flatter and shorter than controls, but were identifiable by their ultrastructure, chemical composition, and thickened tapering morphology. The growth of these dendrites was accompanied by a diminution of MTs from the cell body, indicating a net transfer of MTs from one compartment into the other. During this time, minus-end-distal microtubules arose in the experimental dendrites, indicating that new MT assembly is not required for the acquisition of nonuniform MT polarity orientation in the dendrite. Minus-end-distal microtubules predominated in the more proximal region of experimental dendrites, indicating that most of the MTs at this stage of development are transported into the dendrite with their minus-ends leading. These observations indicate that transport of MTs from the cell body is an essential feature of dendritic development, and that this transport establishes the nonuniform polarity orientation of MTs in the dendrite.

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Grueber, Wesley B., Lily Y. Jan, and Yuh Nung Jan. "Tiling of the Drosophila epidermis by multidendritic sensory neurons." Development 129, no. 12 (June 15, 2002): 2867–78. http://dx.doi.org/10.1242/dev.129.12.2867.

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Insect dendritic arborization (da) neurons provide an opportunity to examine how diverse dendrite morphologies and dendritic territories are established during development. We have examined the morphologies of Drosophila da neurons by using the MARCM (mosaic analysis with a repressible cell marker) system. We show that each of the 15 neurons per abdominal hemisegment spread dendrites to characteristic regions of the epidermis. We place these neurons into four distinct morphological classes distinguished primarily by their dendrite branching complexities. Some class assignments correlate with known proneural gene requirements as well as with central axonal projections. Our data indicate that cells within two morphological classes partition the body wall into distinct, non-overlapping territorial domains and thus are organized as separate tiled sensory systems. The dendritic domains of cells in different classes, by contrast, can overlap extensively. We have examined the cell-autonomous roles of starry night (stan) (also known as flamingo (fmi)) and sequoia (seq) in tiling. Neurons with these genes mutated generally terminate their dendritic fields at normal locations at the lateral margin and segment border, where they meet or approach the like dendrites of adjacent neurons. However, stan mutant neurons occasionally send sparsely branched processes beyond these territories that could potentially mix with adjacent like dendrites. Together, our data suggest that widespread tiling of the larval body wall involves interactions between growing dendritic processes and as yet unidentified signals that allow avoidance by like dendrites.

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

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

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Leung, Donald Y. M., Harold S. Nelson, Stanley J. Szefler, and William W. Busse. "Langerhans cell–like dendritic cells and inflammatory dendritic epidermal cell–like dendritic cells induce distinct T-cell responses." Journal of Allergy and Clinical Immunology 113, no. 5 (May 2004): 803. http://dx.doi.org/10.1016/j.jaci.2004.03.025.

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Dissertations / Theses on the topic "Dendritic cell"

Carnathan, Diane Gail Vilen Barbara J. "Dendritic cell regulation of B cells." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1200.

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Thesis (M.S.)--University of North Carolina at Chapel Hill, 2007.
Title from electronic title page (viewed Mar. 26, 2008). "... in partial fulfillment of the requirements for the degree of Master of Science in the Department of Microbiology and Immunology, School of Medicine." Discipline: Microbiology and Immunology; Department/School: Medicine.

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Liu, Hao. "Dendritic cell development directed by stromal cells." Thesis, University of York, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516409.

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Greensmith, Julie. "The dendritic cell algorithm." Thesis, Nottingham Trent University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444619.

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Kavikondala, Sushma. "Dendritic cell and B cell interactions in systemic lupuserythematosus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39793710.

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Kavikondala, Sushma. "Dendritic cell and B cell interactions in systemic lupus erythematosus." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39711523.

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Rigby, Rachael Jane. "Intestinal dendritic cells : characterisation of the colonic dendritic cell population and identification of potential precursors." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407134.

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Javorovic, Miran. "T-Cell Stimulation by Melanoma RNA-Pulsed Dendritic Cells." Diss., lmu, 2004. http://nbn-resolving.de/urn:nbn:de:bvb:19-30569.

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Pérez, Zsolt Daniel. "New therapeutic strategies targeting dendritic cell-mediated dissemination of enveloped viruses." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/669547.

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Les cèl·lules dendrítiques (DCs) són clau en la inducció de respostes immunitàries adaptatives gràcies a la seva capacitat de capturar, processar i presentar antígens derivats de patògens als limfòcits T. Tanmateix, aquestes cèl·lules podrien contribuir a la disseminació inicial del VIH-1 a través de la captura i transmissió viral a les cèl·lules T CD4+ diana, un procés conegut com a trans-infecció. Aquest mecanisme es basa en l’expressió del receptor Siglec-1 (CD169), que reconeix gangliòsids sialilats a la membrana viral. Els nivells de Siglec-1 augmenten en DCs estimulades amb interferó-alfa i lipopolisacàrid, factors immuno-activadors presents durant el decurs de la infecció per VIH-1. En aquesta tesi, hem demostrat que l’interferó-alfa secretat per DCs plasmacitoides (pDCs) infectades per VIH-1, així com l’inteferó-alfa autocrí secretat per cèl·lules mieloides en resposta a lipopolisacàrid, augmenten l’expressió de Siglec-1 en DCs. A més, les pDCs provinents de dones secreten quantitats superiors d’interferó-alfa que les d’homes, posant de manifest la rellevància d’estudiar la trans-infecció del VIH-1 en teixits clau per a l’adquisició del virus en dones. Així, també hem estudiat el paper de Siglec-1 en la transmissió del VIH-1 per part de DCs primàries aïllades directament de teixit cervical, identificant una població de cèl·lules mieloides cervicals que expressen Siglec-1 i capturen partícules de VIH-1 a través d’aquest receptor. Aquesta capacitat augmenta amb l’activació per interferó-alfa. A més, la transmissió del VIH-1 per cèl·lules mieloides del cèrvix es bloqueja de forma eficient amb un anticòs monoclonal dirigit contra Siglec-1. Per tant, hem generat una sèrie de nous anticossos monoclonals contra Siglec-1 amb la capacitat de bloquejar la tans-infecció del VIH-1 per DCs. S’han produït cinc nous clons, que han demostrat tenir una alta afinitat per diferents epítops localitzats a la regió N-terminal de Siglec-1. A més, aquests anticossos bloquegen la captura i trans-infecció del VIH-1 per DCs, de forma que podrien ser un component en estratègies microbicides dirigides contra aquest tipus de transmissió viral cèl·lula-cèl·lula. A banda del VIH-1, les cèl·lules dendrítiques participen en la patogènesi d’altres virus, com ara els filovirus d’Ebola i Marburg. A diferència del VIH-1, les DCs són permissives a la infecció per filovirus i són dianes primerenques en la patogènesi viral. Els factors cel·lulars implicats en l’entrada de filovirus en aquestes cèl·lules no han estat totalment caracteritzats, però tant Ebola com Marburg són virus embolcallats que incorporen gangliòsids sialilats durant el procés de gemmació viral. A més, els factors que activen l’expressió de Siglec-1 com ara interferó-alfa i lipopolisacàrid s’han trobat durant la infecció pel virus d’Ebola. Per tant, en aquesta tesi hem estudiat el paper de Siglec-1 en l’entrada de filovirus en DCs. Hem trobat que Siglec-1 està implicat en la captura de partícules no infeccioses d’Ebola per part d’aquestes cèl·lules, especialment després de l’activació per interferó-alfa i lipopolisacàrid. A més, les partícules capturades són acumulades en el mateix compartiment cel·lular en què prèviament s’havia detectat el VIH-1. Siglec-1 també facilita l’entrada citoplasmàtica del virus a les DCs, així que hem determinat la capacitat dels nous anticossos monoclonals contra Siglec-1 d’interferir amb aquest procés, i hem vist que aquests bloquegen tant la captura com l’entrada citoplasmàtica de partícules no infeccioses d’Ebola en cèl·lules mieloides activades. En general, l’activitat delsanticossos monoclonals contra Siglec-1 inhibeix l’accés de retrovirus i de filovirus a les cèl·lules mieloides, cosa que indica el seu potencial ús com a agents antivirals d’ampli espectre.
Las células dendríticas (DCs) son clave en la inducción de respestas inmunitarias adaptativas gracias a su capacidad de capturar, procesar y presentar antígenos derivados de patógenos a los linfocitos T. Sin embargo, estas células también podrían contribuir a la diseminación inicial del VIH-1 a través de la captura de partículas virales y de su transmisión a las células T CD4+ diana, un proceso conocido como trans-infección. Este mecanismo se basa en la expresión del receptor Siglec-1 (CD169), que reconoce gangliósidos sialilados en la membrana viral. Los niveles de Siglec-1 aumentan en DCs estimuladas con interferón-alfa (IFN-α) y lipopolisacárido (LPS), factores immuno-activadores presentes durante el curso de la infección por VIH-1. En este trabajo, hemos demostrado que el IFN-α secretado por DCs plasmacitoides (pDCs) infectadas por VIH-1, así como el IFN-α autocrino secretado por células mieloides en respuesta a LPS, aumentan la expresión de Siglec-1 en DCs. Además, las pDCs provenientes de mujeres secretan cantidades superiores de IFN-α que las derivadas de hombres, poniendo de manifiesto la relevancia de estudiar la trans-infección del VIH-1 en tejidos clave para la adquisición del virus en mujeres. Por lo tanto, también hemos estudiado el papel de Siglec-1 en la transmisión del VIH-1 por parte de DCs primarias aisladas directamente de tejido cervical, identificando una población de DCs cervicales que expresan Siglec-1 y capturan partículas de VIH-1 a través de este receptor. Esta capacidad aumenta con la activación por IFN-α. Además, la transmisión célula-célula del VIH-1 por células mieloides del cérvix se puede bloquear de forma eficiente con un anticuerpo monoclonal (mAb) dirigido contra Siglec-1. Se han producido cinco nuevos clones, que han demostrado tener una alta afinidad por diferentes epítopos localizados en la región N-terminal de Siglec-1. Además, bloquean de forma eficaç la captura y trans-infección del VIH-1 por DCs, de forma que podrían ser un posible componente en estrategias microbicidas dirigidas contra este tipo de transmisión viral célula-célula. Además del VIH-1, las DCs pueden jugar un papel importante en la patogénesis de otros virus, como los filovirus Ébola y Marburg. A diferencia del VIH-1, las DCs son permisivas a la infección por filovirus y son dianas tempranas en lapatogénesis viral. Los factores celulares implicados en la entrada de filovirus en DCs no han sido totalmente caracterizados, pero tanto Ébola como Marburg son virus envueltos que incorporan gangliósidos sialilados durante el proceso de budding. Además, los factores que activan la expresión de Siglec-1 como IFN-α y LPS se han encontrado durante la infección por el virus de Ébola. Por tanto, en esta tesis hemos estudiado el papel de Siglec-1 en la entrada de filovirus en DCs. Hemos encontrado que Siglec-1 está implicado en la captura de partículas no infecciosas de Ébola (VLPs) por parte de estas células, especialmente tras la activación por IFN-α y LPS. Además, las VLPs capturadas se acumulan en el mismo compartimento en el que previamente se había detectado VIH-1. Siglec-1 también facilita la entrada citoplásmica del virus en las DCs, así que hemos determinado la capacidad de los nuevos mAbs contra Siglec-1 para interferir en este proceso, y hemos visto que dichos mAbs bloquean tanto la captura como la entrada citoplásmica de VLPs de Ébola en células mieloides activadas. En general, la actividad de los mAbs contra Siglec-1 inhibe el acceso de retrovirus y filovirus en las células mieloides, cosa que indica su potencial uso como agentes antivirales de amplio espectro.
Dendritic cells are key inducers of specific adaptive immune responses due to their capacity to capture, process and present pathogen-derived antigens to T lymphocytes. However, they might also contribute to early HIV-1 dissemination by capturing HIV-1 particles and transmitting them to target CD4+ T cells, a process known as trans-infection. This mechanism relies on the expression of Siglec-1 receptor (CD169), which recognizes sialylated gangliosides on the viral membrane. Siglec-1 is potently up-regulated upon dendritic cell stimulation with interferon-alpha and lipopolysaccharide, which are both immune-activating factors present during the course of HIV-1 infection. Here, we demonstrated that interferon-alpha secreted by HIV-1-infected plasmacytoid dendritic cells and autocrine interferon-alpha secreted by myeloid cells in response to lipopolysaccharide up-regulate Siglec-1 on dendritic cells. Importantly, plasmacytoid dendritic cells derived from women secreted higher amounts of interferon-alpha than those derived from men, highlighting the relevance of studying HIV-1 trans-infection in key female tissues for HIV-1 acquisition. Thus, we next studied the role of Siglec-1 in HIV-1 transmission mediated by primary dendritic cells directly isolated from cervical tissues, identifying a subset of cervical myeloid cells that expressed Siglec-1 and captured HIV-1 particles in a Siglec-1-dependent manner. This capacity was enhanced upon activation with interferon-alpha. Moreover, HIV-1 cell-to-cell transmission mediated by these cells could be efficiently blocked using an anti-Siglec-1 monoclonal antibody, indicating the potential use of antibodies directed against Siglec-1 in prevention of sexually transmitted HIV-1 acquisition in women. Thus, we generated a set of new anti-Siglec-1 monoclonal antibodies with the capacity to block dendritic cell-mediated HIV-1 trans-infection. Five new clones were produced, demonstrating high affinity for different epitopes located in the N-terminal region of Siglec-1 receptor. Moreover, they efficiently blocked HIV-1 capture and trans-infection mediated by dendritic cells, indicating their potential use in microbicidal strategies targeting this type of viral cell-to-cell transmission. Aside from HIV-1, dendritic cells can play important roles in the pathogenesis of other viruses, including Ebola and Marburg filoviruses. In contrast to HIV-1, dendritic cells are permissive to filoviral infection and act as early targets in viral pathogenesis. The host factors governing filoviral entry into these cells are not fully characterized, but both Ebola and Marburg are enveloped viruses that incorporate sialylated gangliosides during the budding process. Moreover, Siglec-1-activating factors such as interferon-alpha and lipopolysaccharide have been found during Ebola virus disease. Thus, we investigated the role of Siglec-1 in filoviral entry into dendritic cells. We found that Siglec-1-mediated capture of non-infectious Ebola virus-like particles into these cells, especially upon interferon-alpha and lipopolysaccharide activation. Interestingly, captured Ebola virus-like particles accumulated in the same cellular compartment where HIV-1 was previously detected. Siglec-1 also facilitated Ebola cytoplasmic entry into dendritic cells, so we tested the capacity of novel anti-Siglec-1 monoclonal antibodies to interfere with this process. We found that capture and cytoplasmic entry of Ebola virus-like particles into activated myeloid cells was blocked by these novel antibodies. Overall, the activity of anti-Siglec-1 monoclonal antibodies inhibits the access of both retroviruses and filoviruses into myeloid cells and suggests their potential use as broad-spectrum antiviral agents.

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Sarris, Milka. "Dynamics of helper T cell and regulatory T cell interactions with dendritic cells." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611896.

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Mahmood, Sajid. "Diverse regulation of natural killer cell functions by dendritic cells." Public Library of Science, 2012. http://hdl.handle.net/1993/23963.

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Natural killer (NK) cells are innate lymphocytes with inherent ability to eliminate infected cells and produce several cytokines/chemokines. They express surface receptors to sense environment and interact with other immune cells including the Dendritic cells (DC). Reciprocally, DCs are also shown to activate NK-cells. NK/DC cross-talk is well-documented, yet the molecular interactions and the diverse NK-cell activities regulated by DC remain unclear. Several target proteins such as MHC-1, Qa-1 mediate NK-cell target recognition. One such antigen, Ocil/Clr-b functions as a cognate ligand of NKR-P1B/D, NK-inhibitory receptor. In first aim of my study, I documented that deficiency of Ocil/Clr-b expression not only augmented the sensitivity of DC towards NK-cell cytotoxicity but also regulated the development of mature NK-cells. Thus suggesting NKR-P1B/D:Ocil to be another receptor:ligand system, besides Ly49:MHC-1, that regulates NK-cell responsiveness. Src homology region 2-containing protein tyrosine phosphatase-1 (SHP-1) transmits inhibitory signals of the specific NK-inhibitory receptors, including NKRP-1B/D. SHP-1 silenced NK-cells showed unaffected target recognition towards prototypic target cells in this study. In addition, these cells also displayed an unexpected phenotype of self-killing in-vitro, thus implicated SHP-1 as an important regulator of some other unappreciated NK-cell functions. The data from my third study suggest that DCs are directly implicated in the induction of NK-cell migration. In summary, using a novel live-cell imaging microfluidic platform and conventional transwell migration assay this project established a clear molecular link between DC-derived soluble factors such as IP-10 and NK cell-chemokine receptor such as CXCR3. Previously, GM-CSF was shown as an inflammatory cytokine, involved in the development of DC as well as in mediating Th-1 immune responses. In this study I found that GM-CSF regulates NK-cell migration negatively. Lastly, the fourth aim of my thesis highlighted the critical role of immature-DC in the induction of maturation receptors (NK1.1 & Ly49) on differentiating NK-cells. I successfully established a multi-stage in-vitro NK-cell differentiation model and found that differentiating NK-cells required an active engagement with DCs, in addition to the soluble factors. I believe my PhD project findings would impact the existing knowledge to harness DC-based NK cell therapies in clinical settings.
October 2014

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Books on the topic "Dendritic cell"

Robinson, Stephen P., and Andrew J. Stagg. Dendritic Cell Protocols. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591507.

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Segura, Elodie, and Nobuyuki Onai, eds. Dendritic Cell Protocols. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3606-9.

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Naik, Shalin H., ed. Dendritic Cell Protocols. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-421-0.

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Rescigno, Maria, ed. Dendritic Cell Interactions with Bacteria. Cambridge: Cambridge University Press, 2001. http://dx.doi.org/10.1017/cbo9780511541551.

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1968-, Rescigno Maria, ed. Dendritic cell interactions with bacteria. Cambridge, UK: Cambridge University Press, 2007.

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Lau, Colleen. Molecular control of dendritic cell development and function. [New York, N.Y.?]: [publisher not identified], 2015.

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Workshop on Langerhans Cells (2nd 1988 Lyon, France). The Langerhans cell =: La cellule de Langerhans : proceedings of the Second Workshop on Langerhans Cells, held in Lyon (France), April 21-22, 1988. Paris, France: Editions INSERM, 1988.

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Jones, David Allan. Dendritic cells, hapten presentation and lymph node cell activation following cutaneous sensitization in the mouse. [s.l.]: typescript, 1991.

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Lewis, Kanako. Targeting of specific developmental pathways to understand dendritic cell heterogeneity and function. [New York, N.Y.?]: [publisher not identified], 2012.

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Greg, Stuart, Spruston Nelson, and Häusser Michael, eds. Dendrites. 2nd ed. Oxford: Oxford University Press, 2007.

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Book chapters on the topic "Dendritic cell"

Tew, John G. "Follicular Dendritic Cells and Dendritic Cell Nomenclature." In Advances in Experimental Medicine and Biology, 467–68. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2930-9_78.

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Rosenblatt, Jacalyn, and David Avigan. "Dendritic Cells." In Allogeneic Stem Cell Transplantation, 807–54. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-478-0_45.

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Avigan, David. "Dendritic Cells." In Allogeneic Stem Cell Transplantation, 411–38. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-333-0_26.

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Ylagan, Lourdes R. "Dendritic Cell Tumors." In Dendritic Cells in Cancer, 365–74. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-88611-4_24.

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Kreitinger, Joanna M., and David M. Shepherd. "Dendritic Cell Assays." In Methods in Molecular Biology, 243–53. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8549-4_16.

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Dhodapkar, Madhav V. "Dendritic Cell Vaccines." In Handbook of Cancer Vaccines, 317–29. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-680-5_21.

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Sabado, Rachel Lubong, Marcia Meseck, and Nina Bhardwaj. "Dendritic Cell Vaccines." In Vaccine Design, 763–77. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3387-7_44.

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Thurnher, Martin. "Dendritic Cell Vaccines." In Allergy Frontiers: Future Perspectives, 267–76. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99365-0_17.

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Schachter, Levanto. "Dendritic Cell Vaccines." In Blood and Marrow Transplant Handbook, 895–903. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-53626-8_56.

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Yamanaka, Ryuya, and Koji Kajiwara. "Dendritic Cell Vaccines." In Advances in Experimental Medicine and Biology, 187–200. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3146-6_15.

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Conference papers on the topic "Dendritic cell"

Lutfi, Riad, John R. Ledford, Ping Zhou, and Kristen Page. "Dendritic Cell Reprogramming Of Airway Epithelial Cell Responses." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1065.

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Braun, Armin, Emma Spies, Sabine Rochlitzer, and Sabrina Voedisch. "Neuropeptides Influence Airway Dendritic Cell Behavior." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2155.

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Desch, Ashley N., Gwendalyn J. Randolph, Robert J. Mason, Peter M. Henson, and Claudia Jakubzick. "Pulmonary Dendritic Cell Specificity Of Efferocytosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2838.

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Zhang, Yujie. "Dendritic cell vaccine in cancer immunotherapy." In Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), edited by Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3013149.

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Xu, Q. Y., W. M. Feng, and B. C. Liu. "3D Stochastic Modeling of As-Cast Microstructure for Aluminum Alloy Casting." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32894.

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A 3D stochastic modeling was carried out to simulate the dendritic grains during solidification process of aluminum alloy, including time-dependent calculations for temperature field, solute redistribution in liquid, curvature of the dendritic tip, and growth anisotropy. The nucleation process was calculated by continuous nucleation. A 3D simplified grain shape model was established to represent the equiaxed dendritic grain. Based on the Cellular Automaton method, a grain growth model was proposed to capture the neighbor cells of the nucleated cell. On growing, each grain continues to capture the nearest neighbor cells to form the final shape. When a neighboring cell has been captured by the other grains, the grain growth along this direction is stopped. Three-dimensional calculations were performed to simulate the evolution of dendritic grain. In order to verify the modeling results, aluminum alloy sample castings were cast in sand and metal mold.

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Stibor, Thomas, Robert Oates, Graham Kendall, and Jonathan M. Garibaldi. "Geometrical insights into the dendritic cell algorithm." In the 11th Annual conference. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1569901.1570072.

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Fu, Jun, Yiwen Liang, Chengyu Tan, and Xiaofei Xiong. "Detecting Software Keyloggers with Dendritic Cell Algorithm." In 2010 International Conference on Communications and Mobile Computing (CMC). IEEE, 2010. http://dx.doi.org/10.1109/cmc.2010.269.

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Crockett, Caroline, Elizabeth Orrico, Sara McArdle, Klaus Ley, and Scott T. Acton. "Momentum measure for quantifying dendritic cell movement." In 2015 49th Asilomar Conference on Signals, Systems and Computers. IEEE, 2015. http://dx.doi.org/10.1109/acssc.2015.7421275.

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Zhou, Wen, Yiwen Liang, Hongbin Dong, Chengyu Tan, Zhenhua Xiao, and Weiwei Liu. "A Numerical Differentiation Based Dendritic Cell Model." In 2017 IEEE 29th International Conference on Tools with Artificial Intelligence (ICTAI). IEEE, 2017. http://dx.doi.org/10.1109/ictai.2017.00167.

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Greensmith, Julie, and Longzhi Yang. "TwoDCA: A 2-Dimensional Dendritic Cell Algorithm with Dynamic Cell Migration." In 2022 IEEE Congress on Evolutionary Computation (CEC). IEEE, 2022. http://dx.doi.org/10.1109/cec55065.2022.9870441.

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Reports on the topic "Dendritic cell"

Easoz, J., R. Rosey, R. Campbell, R. Rupnik, R. Sprecace, P. Piotrowski, J. McHugh, and R. Seidensticker. Dendritic web silicon photovoltaic cell research. Office of Scientific and Technical Information (OSTI), May 1990. http://dx.doi.org/10.2172/6904462.

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Akporiaye, Emmanuel T. Tumor-Mediated Suppression of Dendritic Cell Vaccines. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada428247.

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Mathis, James M. Dendritic Cell-Based Genetic Immunotherapy for Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada491946.

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Mathis, James M. Dendritic Cell-Based Genetic Immunotherapy for Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2008. http://dx.doi.org/10.21236/ada518244.

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Mathis, James M. Dendritic Cell-Based Genetic Immunotherapy for Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada462730.

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Gilboa, Eli. Immunotherapy of Breast with Tumor RNA Transfected Dendritic Cell Vaccines. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada398155.

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Baar, Joseph. Dendritic Cell-Based Immunotherapy of Breast Cancer: Modulation by CpG. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada431640.

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Dewhurst, Stephen. Dendritic Cell-Targeted Phage Vectors for Breast Cancer Vaccine Development. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417050.

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Ramanathapuram, Lalitha V., and Emmanuel T. Akporiaye. Vitamin E Succinate as an Adjuvant for Dendritic Cell-Based Vaccines. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada443920.

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Odegard, Elin. Dendritic Cell-Targeted Vaccinations: A Promising Immunotherapeutic Approach to Cancer Treatment. Portland State University Library, January 2015. http://dx.doi.org/10.15760/honors.148.

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