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1
Velte, Toby J., and Richard H. Masland. "Action Potentials in the Dendrites of Retinal Ganglion Cells." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 1412–17. http://dx.doi.org/10.1152/jn.1999.81.3.1412.
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Action potentials in the dendrites of retinal ganglion cells. The somas and dendrites of intact retinal ganglion cells were exposed by enzymatic removal of the overlying endfeet of the Müller glia. Simultaneous whole cell patch recordings were made from a ganglion cell’s dendrite and the cell’s soma. When a dendrite was stimulated with depolarizing current, impulses often propagated to the soma, where they appeared as a mixture of small depolarizations and action potentials. When the soma was stimulated, action potentials always propagated back through the dendrite. The site of initiation of action potentials, as judged by their timing, could be shifted between soma and dendrite by changing the site of stimulation. Applying QX-314 to the soma could eliminate somatic action potentials while leaving dendritic impulses intact. The absolute amplitudes of the dendritic action potentials varied somewhat at different distances from the soma, and it is not clear whether these variations are real or technical. Nonetheless, the qualitative experiments clearly suggest that the dendrites of retinal ganglion cells generate regenerative Na+ action potentials, at least in response to large direct depolarizations.
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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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Cazé, Romain D. "Any neuron can perform linearly non-separable computations." F1000Research 10 (July 6, 2021): 539. http://dx.doi.org/10.12688/f1000research.53961.1.
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Multiple studies have shown how dendrites enable some neurons to perform linearly non-separable computations. These works focus on cells with an extended dendritic arbor where voltage can vary independently, turning dendritic branches into local non-linear subunits. However, these studies leave a large fraction of the nervous system unexplored. Many neurons, e.g. granule cells, have modest dendritic trees and are electrically compact. It is impossible to decompose them into multiple independent subunits. Here, we upgraded the integrate and fire neuron to account for saturating dendrites. This artificial neuron has a unique membrane voltage and can be seen as a single layer. We present a class of linearly non-separable computations and how our neuron can perform them. We thus demonstrate that even a single layer neuron with dendrites has more computational capacity than without. Because any neuron has one or more layer, and all dendrites do saturate, we show that any dendrited neuron can implement linearly non-separable computations.
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Cazé, Romain D. "Any neuron can perform linearly non-separable computations." F1000Research 10 (September 16, 2021): 539. http://dx.doi.org/10.12688/f1000research.53961.2.
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Multiple studies have shown how dendrites enable some neurons to perform linearly non-separable computations. These works focus on cells with an extended dendritic arbor where voltage can vary independently, turning dendritic branches into local non-linear subunits. However, these studies leave a large fraction of the nervous system unexplored. Many neurons, e.g. granule cells, have modest dendritic trees and are electrically compact. It is impossible to decompose them into multiple independent subunits. Here, we upgraded the integrate and fire neuron to account for saturating dendrites. This artificial neuron has a unique membrane voltage and can be seen as a single layer. We present a class of linearly non-separable computations and how our neuron can perform them. We thus demonstrate that even a single layer neuron with dendrites has more computational capacity than without. Because any neuron has one or more layer, and all dendrites do saturate, we show that any dendrited neuron can implement linearly non-separable computations.
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Yanagawa, Yoshiki, and Kazunori Onoé. "CCL19 induces rapid dendritic extension of murine dendritic cells." Blood 100, no. 6 (September 15, 2002): 1948–56. http://dx.doi.org/10.1182/blood-2002-01-0260.
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Abstract Dendritic cells (DCs) possess numerous dendrites that may be of great advantage to interaction with T cells. However, it has been poorly understood how the dendritic morphology of a DC is controlled. In the present study, using a murine spleen-derived DC line, we analyzed effects of CCR7 ligands, CCL19 and CCL21, on dendritic morphology. Mature DCs, but not immature DCs, showed vigorous migration to either CCL19 or CCL21. CCL19 also rapidly (within 30 minutes) induced marked extension of dendrites of mature DCs that was maintained at least for 24 hours. On the other hand, CCL21 failed to induce rapid dendritic extension, even though a modest dendritic extension of mature DCs, compared to that by CCL19, was induced 8 or 24 hours after treatment with CCL21. In addition, pretreatment with a high concentration of CCL21 significantly inhibited the rapid dendritic extension induced by CCL19. Thus, it is suggested that CCL19 and CCL21 exert agonistic and antagonistic influences on the initiation of dendritic extension of mature DCs. The CCL19-induced morphologic changes were completely blocked by Clostridium difficiletoxin B that inhibits Rho guanosine triphosphatase proteins such as Rho, Rac, and Cdc42, but not by Y-27632, a specific inhibitor for Rho-associated kinase. These findings suggest that Rac or Cdc42 (or both), but not Rho, are involved in the CCL19-induced dendritic extension of mature DCs.
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Ulrich, Daniel. "Dendritic Resonance in Rat Neocortical Pyramidal Cells." Journal of Neurophysiology 87, no. 6 (June 1, 2002): 2753–59. http://dx.doi.org/10.1152/jn.2002.87.6.2753.
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Dendritic integration of synaptic signals is likely to be an important process by which nerve cells encode synaptic input into spike output. However, the response properties of dendrites to time-varying inputs are largely unknown. Here, I determine the transfer impedance of the apical dendrite in layer V pyramidal cells by dual whole cell patch-clamp recordings in slices of rat somatosensory cortex. Sinusoidal current waveforms of linearly changing frequencies (0.1–25 Hz) were alternately injected into the soma or apical dendrite and the resulting voltage oscillations recorded by the second electrode. Dendrosomatic and somatodendritic transfer impedances were calculated by Fourier analysis. At near physiological temperatures ( T∼35°C), the transfer impedance had a maximal magnitude at low frequencies ( f res ∼6 Hz). In addition, voltage led current up to ∼3 Hz, followed by a current lead over voltage at higher frequencies. Thus the transfer impedance of the apical dendrite is characterized by a low-frequency resonance. The frequency of the resonance was voltage dependent, and its strength increased with dendritic distance. The resonance was completely abolished by the I h channel blocker ZD 7288. Dendrosomatic and somatodendritic transfer properties of the apical dendrite were independent of direction or amplitude of the input current, and the responses of individual versus distributed inputs were additive, thus implying linearity. For just threshold current injections, action potentials were generated preferentially at the resonating frequency. I conclude that due to the interplay of a sag current ( I h) with the membrane capacitance, layer V pyramids can act as linear band-pass filters with a frequency preference in the theta frequency band.
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Schwindt, Peter, and Wayne Crill. "Mechanisms Underlying Burst and Regular Spiking Evoked by Dendritic Depolarization in Layer 5 Cortical Pyramidal Neurons." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 1341–54. http://dx.doi.org/10.1152/jn.1999.81.3.1341.
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Mechanisms underlying burst and regular spiking evoked by dendritic depolarization in layer 5 cortical pyramidal neurons. Apical dendrites of layer 5 pyramidal cells in a slice preparation of rat sensorimotor cortex were depolarized focally by long-lasting glutamate iontophoresis while recording intracellularly from their soma. In most cells the firing pattern evoked by the smallest dendritic depolarization that evoked spikes consisted of repetitive bursts of action potentials. During larger dendritic depolarizations initial burst firing was followed by regular spiking. As dendritic depolarization was increased further the duration (but not the firing rate) of the regular spiking increased, and the duration of burst firing decreased. Depolarization of the soma in most of the same cells evoked only regular spiking. When the dendrite was depolarized to a critical level below spike threshold, intrasomatic current pulses or excitatory postsynaptic potentials also triggered bursts instead of single spikes. The bursts were driven by a delayed depolarization (DD) that was triggered in an all-or-none manner along with the first Na+ spike of the burst. Somatic voltage-clamp experiments indicated that the action current underlying the DD was generated in the dendrite and was Ca2+ dependent. Thus the burst firing was caused by a Na+ spike-linked dendritic Ca2+spike, a mechanism that was available only when the dendrite was adequately depolarized. Larger dendritic depolarization that evoked late, constant-frequency regular spiking also evoked a long-lasting, Ca2+-dependent action potential (a “plateau”). The duration of the plateau but not its amplitude was increased by stronger dendritic depolarization. Burst-generating dendritic Ca2+spikes could not be elicited during this plateau. Thus plateau initiation was responsible for the termination of burst firing and the generation of the constant-frequency regular spiking. We conclude that somatic and dendritic depolarization can elicit quite different firing patterns in the same pyramidal neuron. The burst and regular spiking observed during dendritic depolarization are caused by two types of Ca2+-dependent dendritic action potentials. We discuss some functional implications of these observations.
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Larkum, M. E., M. G. Rioult, and H. R. Luscher. "Propagation of action potentials in the dendrites of neurons from rat spinal cord slice cultures." Journal of Neurophysiology 75, no. 1 (January 1, 1996): 154–70. http://dx.doi.org/10.1152/jn.1996.75.1.154.
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1. We examined the propagation of action potentials in the dendrites of ventrally located presumed motoneurons of organotypic rat spinal cord cultures. Simultaneous patch electrode recordings were made from the dendrites and somata of individual cells. In other experiments we visualized the membrane voltage over all the proximal dendrites simultaneously using a voltage-sensitive dye and an array of photodiodes. Calcium imaging was used to measure the dendritic rise in Ca2+ accompanying the propagating action potentials. 2. Spontaneous and evoked action potentials were recorded using high-resistance patch electrodes with separations of 30-423 microm between the somatic and dendritic electrodes. 3. Action potentials recorded in the dendrites varied considerably in amplitude but were larger than would be expected if the dendrites were to behave as passive cables (sometimes little or no decrement was seen for distances of > 100 microm). Because the amplitude of the action potentials in different dendrites was not a simple function of distance from the soma, we suggest that the conductance responsible for the boosting of the action potential amplitude varied in density from dendrite to dendrite and possibly along each dendrite. 4. The dendritic action potentials were usually smaller and broader and arrived later at the dendritic electrode than at the somatic electrode irrespective of whether stimulation occurred at the dendrite or soma or as a result of spontaneous synaptic activity. This is clear evidence that the action potential is initiated at or near the soma and spreads out into the dendrites. The conduction velocity of the propagating action potential was estimated to be 0.5 m/s. 5. The voltage time courses of previously recorded action potentials were generated at the soma using voltage clamp before and after applying 1 microM tetrodotoxin (TTX) over the soma and dendrites. TTX reduced the amplitude of the action potential at the dendritic electrode to a value in the range expected for dendrites that behave as passive cables. This indicates that the conductance responsible for the actively propagating action potentials is a Na+ conductance. 6. The amplitude of the dendritic action potential could also be initially reduced more than the somatic action potential using 1-10 mM QX-314 (an intracellular sodium channel blocker) in the dendritic electrode as the drug diffused from the dendritic electrode toward the soma. Furthermore, in some cases the action potential elicited by current injection into the dendrite had two components. The first component was blocked by QX-314 in the first few seconds of the diffusion of the blocker. 7. In some cells, an afterdepolarizing potential (ADP) was more prominent in the dendrite than in the soma. This ADP could be reversibly blocked by 1 mM Ni2+ or by perfusion of a nominally Ca2+-free solution over the soma and dendrites. This suggests that the back-propagating action potential caused an influx of Ca2+ predominantly in the dendrites. 8. With the use of a voltage-sensitive dye (di-8-ANEPPS) and an array of photodiodes, the action potential was tracked along all the proximal dendrites simultaneously. The results confirmed that the action potential propagated actively, in contrast to similarly measured hyperpolarizing pulses that spread passively. There were also indications that the action potential was not uniformly propagated in all the dendrites, suggesting the possibility that the distribution of Na+ channels over the dendritic membrane is not uniform. 9. Calcium imaging with the Ca2+ fluorescent indicator Fluo-3 showed a larger percentage change in fluorescence in the dendrites than in the soma. Both bursts and single action potentials elicited sharp rises in fluorescence in the proximal dendrites, suggesting that the back-propagating action potential causes a concomitant rise in intracellular calcium concentration...
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Szakal, A. K., R. L. Gieringer, M. H. Kosco, and J. G. Tew. "Isolated follicular dendritic cells: cytochemical antigen localization, Nomarski, SEM, and TEM morphology." Journal of Immunology 134, no. 3 (March 1, 1985): 1349–59. http://dx.doi.org/10.4049/jimmunol.134.3.1349.
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Abstract The objectives of the present study were to determine the cytological features of isolated follicular dendritic cells (FDC), which distinguish them from other leukocytes or dendritic cell types. Consequently, we have developed methods for the fixation, peroxidase cytochemistry, and visualization of FDC, which are applicable to cytological evaluations by Nomarski optics, scanning, and transmission electron microscopy. A functionally supported identification of FDC in vitro was made possible by utilizing, in conjunction with the dendritic morphology, the cytochemically identifiable antigen, horseradish peroxidase (HRP), and the known capacity of FDC to sequester immune complexes (i.e. HRP-anti-HRP) on their plasma membranes. The observations showed that FDC constitute a relatively pleomorphic, nonphagocytic group, distinct from other dendritic type cells such as lymphoid dendritic cells, Langerhans cells, and interdigitating cells (LDC, LC, and IDC), as well as typical leukocytes. Morphologically distinct FDC were identified as cells either with filiform dendrites or with "beaded" dendrites. FDC possessed a single or sometimes a double, lymphocyte-size cell body, which contained an irregular, lobated nucleus, Golgi apparatus, numerous small vesicles, and some mitochondria. Mitochondria were not abundant in the dendritic processes. Filiform dendrites tended to branch and anastomose near the cell body and form a radiating "sunburst"-like pattern. On the average, dendrites measured 15-20 microns in length and 0.1-0.3 micron in diameter. Occasional dendrites were extremely elongated, reached several hundred microns in length, and terminated in an enlargement measuring nearly a micron in diameter. Other filiform dendrites usually had a club-shaped terminal enlargement. The microspheres of "beaded" dendrites ranged between 0.3 and 0.6 micron in diameter. The dendritic processes were also shown to have a highly ordered pattern of immune complex attachment on their surface, suggestive of a periodic arrangement of receptor sites.
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Hamze, Kassem, Sabine Autret, Krzysztof Hinc, Soumaya Laalami, Daria Julkowska, Romain Briandet, Margareth Renault, et al. "Single-cell analysis in situ in a Bacillus subtilis swarming community identifies distinct spatially separated subpopulations differentially expressing hag (flagellin), including specialized swarmers." Microbiology 157, no. 9 (September 1, 2011): 2456–69. http://dx.doi.org/10.1099/mic.0.047159-0.
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The non-domesticated Bacillus subtilis strain 3610 displays, over a wide range of humidity, hyper-branched, dendritic, swarming-like migration on a minimal agar medium. At high (70 %) humidity, the laboratory strain 168 sfp + (producing surfactin) behaves very similarly, although this strain carries a frameshift mutation in swrA, which another group has shown under their conditions (which include low humidity) is essential for swarming. We reconcile these different results by demonstrating that, while swrA is essential for dendritic migration at low humidity (30–40 %), it is dispensable at high humidity. Dendritic migration (flagella- and surfactin-dependent) of strains 168 sfp + swrA and 3610 involves elongation of dendrites for several hours as a monolayer of cells in a thin fluid film. This enabled us to determine in situ the spatiotemporal pattern of expression of some key players in migration as dendrites develop, using gfp transcriptional fusions for hag (encoding flagellin), comA (regulation of surfactin synthesis) as well as eps (exopolysaccharide synthesis). Quantitative (single-cell) analysis of hag expression in situ revealed three spatially separated subpopulations or cell types: (i) networks of chains arising early in the mother colony (MC), expressing eps but not hag; (ii) largely immobile cells in dendrite stems expressing intermediate levels of hag; and (iii) a subpopulation of cells with several distinctive features, including very low comA expression but hyper-expression of hag (and flagella). These specialized cells emerge from the MC to spearhead the terminal 1 mm of dendrite tips as swirling and streaming packs, a major characteristic of swarming migration. We discuss a model for this swarming process, emphasizing the importance of population density and of the complementary roles of packs of swarmers driving dendrite extension, while non-mobile cells in the stems extend dendrites by multiplication.
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BANCHEREAU, JACQUES, SOPHIE PACZESNY, PATRICK BLANCO, LYNDA BENNETT, VIRGINIA PASCUAL, JOSEPH FAY, and A. KAROLINA PALUCKA. "Dendritic Cells." Annals of the New York Academy of Sciences 987, no. 1 (April 2003): 180–87. http://dx.doi.org/10.1111/j.1749-6632.2003.tb06047.x.
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Ardavı́n, Carlos, Sebastián Amigorena, and Caetano Reis e Sousa. "Dendritic Cells." Immunity 20, no. 1 (January 2004): 17–23. http://dx.doi.org/10.1016/s1074-7613(03)00352-2.
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Di Nicola, Massimo, and A. Massimo Gianni. "Dendritic Cells." Tumori Journal 1, no. 6_suppl1 (November 2002): S29—S31. http://dx.doi.org/10.1177/03008916020016s110.
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Mellman, Ira, and Ralph M. Steinman. "Dendritic Cells." Cell 106, no. 3 (August 2001): 255–58. http://dx.doi.org/10.1016/s0092-8674(01)00449-4.
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Rigley, Kevin. "Dendritic Cells." Immunology Today 21, no. 3 (March 2000): 156–57. http://dx.doi.org/10.1016/s0167-5699(00)01602-9.
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Telser, Alvin. "DENDRITIC CELLS." Shock 12, no. 6 (December 1999): 480. http://dx.doi.org/10.1097/00024382-199912000-00014.
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Austyn, Jonathan M. "Dendritic cells." Current Opinion in Hematology 5, no. 1 (January 1998): 3–15. http://dx.doi.org/10.1097/00062752-199801000-00002.
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Yao, Veronica, Cameron Platell, and John C. Hall. "Dendritic cells." ANZ Journal of Surgery 72, no. 7 (July 2002): 501–6. http://dx.doi.org/10.1046/j.1445-2197.2002.02450.x.
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Palucka, Karolina, Hideki Ueno, Lee Roberts, Joseph Fay, and Jacques Banchereau. "Dendritic Cells." Cancer Journal 16, no. 4 (July 2010): 318–24. http://dx.doi.org/10.1097/ppo.0b013e3181eaca83.
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Schuler, Gerold. "Dendritic Cells." Cancer Journal 17, no. 5 (September 2011): 337–42. http://dx.doi.org/10.1097/ppo.0b013e3182350077.
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Oertner, Thomas G., Tilmann M. Brotz, and Alexander Borst. "Mechanisms of Dendritic Calcium Signaling in Fly Neurons." Journal of Neurophysiology 85, no. 1 (January 1, 2001): 439–47. http://dx.doi.org/10.1152/jn.2001.85.1.439.
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We examined the mechanisms underlying dendritic calcium accumulation in lobula plate tangential cells of the fly visual system using an in vitro preparation of the fly brain. Local visual stimulation evokes a localized calcium signal in the dendrites of these cells in vivo. Here we show that a similar localized calcium accumulation can be elicited in vitro by focal iontophoretic application of the cholinergic agonist carbachol. The calcium signal had at least two sources: first, voltage-dependent calcium channels contributed to the carbachol-induced signal and were concentrated on the dendrite, the soma, and the terminal ramification of the axon. However, the dendritic calcium signal induced by carbachol stimulation was only weakly dependent on membrane depolarization. The most likely explanation for the second, voltage-independent part of the dendritic calcium signal is calcium entry through nicotinic acetylcholine receptors. We found no indication of second-messenger or calcium-mediated calcium release from intracellular stores. In summary, the characteristic spatiotemporal calcium signals in the dendrites of lobula plate tangential cells can be reproduced in vitro, and result from a combination of voltage- and ligand-gated calcium influx.
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PETERSON, BETH B., and DENNIS M. DACEY. "Morphology of wide-field bistratified and diffuse human retinal ganglion cells." Visual Neuroscience 17, no. 4 (July 2000): 567–78. http://dx.doi.org/10.1017/s0952523800174073.
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To study the detailed morphology of human retinal ganglion cells, we used intracellular injection of horseradish peroxidase and Neurobiotin to label over 1000 cells in an in vitro, wholemount preparation of the human retina. This study reports on the morphology of 119 wide-field bistratified and 42 diffuse ganglion cells. Cells were analyzed quantitatively on the basis of dendritic-field size, soma size, and the extent of dendritic branching. Bistratified cells were similar in dendritic-field diameter (mean ± s.d. = 682 ± 130 μm) and soma diameter (mean ± s.d. = 18 ± 3.3 μm) but showed a broad distribution in the extent of dendritic branching (mean ± s.d. branch point number = 67 ± 32; range = 15–167). Differences in the extent of branching and in dendritic morphology and the pattern of branching suggest that the human retina may contain at least three types of wide-field bistratified cells. Diffuse ganglion cells comprised a largely homogeneous group whose dendrites ramified throughout the inner plexiform layer. The diffuse cells had similar dendritic-field diameters (mean ± s.d. = 486 ± 113 μm), soma diameters (mean ± s.d. = 16 ± 2.3 μm), and branch points numbers (mean ± s.d. = 92 ± 32). The majority had densely branched dendritic trees and thin, very spiny dendrites with many short, fine, twig-like thorny processes. Five of the diffuse cells had much more sparsely branched dendritic trees (<50 branch points) and less spiny dendrites, suggesting that there are possibly two types of diffuse ganglion cells in human retina. Although the presence of a diversity of large bistratified and diffuse ganglion cells has been observed in a variety of mammalian retinas, little is known about the number of cell types, their physiological properties, or their central projections. Some of the human wide-field bistratified cells in the present study, however, show morphological similarities to monkey large bistratified cells that are known to project to the superior colliculus.
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Zagha, Edward, Satoshi Manita, William N. Ross, and Bernardo Rudy. "Dendritic Kv3.3 Potassium Channels in Cerebellar Purkinje Cells Regulate Generation and Spatial Dynamics of Dendritic Ca2+ Spikes." Journal of Neurophysiology 103, no. 6 (June 2010): 3516–25. http://dx.doi.org/10.1152/jn.00982.2009.
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Purkinje cell dendrites are excitable structures with intrinsic and synaptic conductances contributing to the generation and propagation of electrical activity. Voltage-gated potassium channel subunit Kv3.3 is expressed in the distal dendrites of Purkinje cells. However, the functional relevance of this dendritic distribution is not understood. Moreover, mutations in Kv3.3 cause movement disorders in mice and cerebellar atrophy and ataxia in humans, emphasizing the importance of understanding the role of these channels. In this study, we explore functional implications of this dendritic channel expression and compare Purkinje cell dendritic excitability in wild-type and Kv3.3 knockout mice. We demonstrate enhanced excitability of Purkinje cell dendrites in Kv3.3 knockout mice, despite normal resting membrane properties. Combined data from local application pharmacology, voltage clamp analysis of ionic currents, and assessment of dendritic Ca2+ spike threshold in Purkinje cells suggest a role for Kv3.3 channels in opposing Ca2+ spike initiation. To study the physiological relevance of altered dendritic excitability, we measured [Ca2+]i changes throughout the dendritic tree in response to climbing fiber activation. Ca2+ signals were specifically enhanced in distal dendrites of Kv3.3 knockout Purkinje cells, suggesting a role for dendritic Kv3.3 channels in regulating propagation of electrical activity and Ca2+ influx in distal dendrites. These findings characterize unique roles of Kv3.3 channels in dendrites, with implications for synaptic integration, plasticity, and human disease.
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Velte, T. J., and R. F. Miller. "Spiking and nonspiking models of starburst amacrine cells in the rabbit retina." Visual Neuroscience 14, no. 6 (November 1997): 1073–88. http://dx.doi.org/10.1017/s0952523800011780.
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AbstractThe integrative properties of starburst amacrine cells in the rabbit retina were studied with compartmental models and computer-simulation techniques. The anatomical basis for these simulations was provided by computer reconstructions of intracellularly stained starburst amacrine cells and published data on dendritic diameter and biophysical properties. Passive and active membrane properties were included to simulate spiking and nonspiking behavior. Simulated synaptic inputs into one or more compartments consisted of a bipolar-like conductance change with peak and steady-state components provided by the sum of two Gaussian responses. Simulated impulse generation was achieved by using a model of impulse generation that included five nonlinear channels (INa, ICa, Ia,. Ik. Ik.Ca). The magnitude of the sodium channel conductance change was altered to meet several different types of impulse generation and propagation behaviors. We studied a range of model constraints which included variations in membrane resistance (Rm) from 4,000 Ω.cm2 to 100,000 Ω.cm2, and dendritic diameter from 0.1 to 0.3 μm. In a separate series of simulations, we studied the feasibility of voltage-clamping starburst amacrine cells using a soma-applied, single-electrode voltage clamp, based on models with and without dendritic and somatic spiking behavior. Our simulation studies suggest that single dendrites of starburst amacrine cells can behave as independent functional subunits when the Rm is high, provided that one or a small number of dendrites is synaptically co-activated. However, as the number of co-activated dendrites increases, the starburst cell behavior becomes more uniform and independent dendritic function is less prevalent. The presence of impulse activity in the dendrites raises new questions about dendritic function. However, dendritic impulses do not necessarily eliminate independent dendritic function, because dendritic impulses commonly fail as they propagate toward the soma, where they contribute EPSP-like responses which summate with conventional synaptic currents.
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Hitchcock, P. F. "Exclusionary dendritic interactions in the retina of the goldfish." Development 106, no. 3 (July 1, 1989): 589–98. http://dx.doi.org/10.1242/dev.106.3.589.
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The retina of the goldfish grows throughout its life, in part, by the addition of new neurons at the margin. New ganglion cells added at the margin tend not to grow their dendritic arbors into the older, central retina. Hitchcock and Easter (J. Neurosci. 6, 1037–1050 (1986)) proposed that the dendrites of the new cells were prevented from extending centrally within the inner plexiform layer by the dendrites of the previous generations of cells. This proposal was tested by first killing existing ganglion cells with a retrogradely transported neurotoxin (propidium iodide; PI), and then observing the orientation and branching pattern of the dendrites of ganglion cells added subsequently at the margin. Dendrites were stained in retinal wholemounts by intracellular injections of Lucifer yellow. The data showed that cells added subsequent to the PI treatment grew their dendritic arbors preferentially toward central retina consistent with the hypothesis. It is concluded that interactions among adjacent ganglion cells regulates dendritic growth.
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Cho, Kwang-Hyun, Jin Hwa Jang, Hyun-Jong Jang, Myung-Jun Kim, Shin Hee Yoon, Takaichi Fukuda, Frank Tennigkeit, Wolf Singer, and Duck-Joo Rhie. "Subtype-Specific Dendritic Ca2+ Dynamics of Inhibitory Interneurons in the Rat Visual Cortex." Journal of Neurophysiology 104, no. 2 (August 2010): 840–53. http://dx.doi.org/10.1152/jn.00146.2010.
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The Ca2+ increase in dendrites that is evoked by the backpropagation of somatic action potentials (APs) is involved in the activity-dependent modulation of dendritic and synaptic functions that are location dependent. In the present study, we investigated dendritic Ca2+ dynamics evoked by backpropagating APs (bAPs) in four subtypes of inhibitory interneurons classified by their spiking patterns: fast spiking (FS), late spiking (LS), burst spiking (BS), and regular-spiking nonpyramidal (RSNP) cells. Cluster analysis, single-cell RT-PCR, and immunohistochemistry confirmed the least-overlapping nature of the grouped cell populations. Somatic APs evoked dendritic Ca2+ transients in all subtypes of inhibitory interneurons with different spatial profiles along the tree: constantly linear in FS and LS cells, increasing to a plateau in BS cells and bell-shaped in RSNP cells. The increases in bAP-evoked dendritic Ca2+ transients brought about by the blocking of A-type K+ channels were similar in whole dendritic trees of each subtype of inhibitory interneurons. However, in RSNP cells, the increases in the distal dendrites were larger than those in the proximal dendrites. On cholinergic activation, nicotinic inhibition of bAP-evoked dendritic Ca2+ transients was observed only in BS cells expressing cholecystokinin and vasoactive intestinal peptide mRNAs, with no muscarinic modulation in all subtypes of inhibitory interneurons. Cell subtype-specific differential spatial profiles and their modulation in bAP-evoked dendritic Ca2+ transients might be important for the domain-specific modulation of segregated inputs in inhibitory interneurons and differential control between the excitatory and inhibitory networks in the visual cortex.
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Lüscher, Hans-R., and Matthew E. Larkum. "Modeling Action Potential Initiation and Back-Propagation in Dendrites of Cultured Rat Motoneurons." Journal of Neurophysiology 80, no. 2 (August 1, 1998): 715–29. http://dx.doi.org/10.1152/jn.1998.80.2.715.
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Lüscher, Hans-R. and Matthew E. Larkum. Modeling action potential initiation and back-propagation in dendrites of cultured rat motoneurons. J. Neurophysiol. 80: 715–729, 1998. Regardless of the site of current injection, action potentials usually originate at or near the soma and propagate decrementally back into the dendrites. This phenomenon has been observed in neocortical pyramidal cells as well as in cultured motoneurons. Here we show that action potentials in motoneurons can be initiated in the dendrite as well, resulting in a biphasic dendritic action potential. We present a model of spinal motoneurons that is consistent with observed physiological properties of spike initiation in the initial segment/axon hillock region and action potential back-propagation into the dendritic tree. It accurately reproduces the results presented by Larkum et al. on motoneurons in organotypic rat spinal cord slice cultures. A high Na+-channel density of ḡ Na = 700 mS/cm2 at the axon hillock/initial segment region was required to secure antidromic invasion of the somato-dendritic membrane, whereas for the orthodromic direction, a Na+-channel density of ḡ Na = 1,200 mS/cm2 was required. A “weakly” excitable ( ḡ Na = 3 mS/cm2) dendritic membrane most accurately describes the experimentally observed attenuation of the back-propagated action potential. Careful analysis of the threshold conditions for action potential initiation at the initial segment or the dendrites revealed that, despite the lower voltage threshold for spike initiation in the initial segment, an action potential can be initiated in the dendrite before the initial segment fires a spike. Spike initiation in the dendrite depends on the passive cable properties of the dendritic membrane, its Na+-channel density, and local structural properties, mainly the diameter of the dendrites. Action potentials are initiated more easily in distal than in proximal dendrites. Whether or not such a dendritic action potential invades the soma with a subsequent initiation of a second action potential in the initial segment depends on the actual current source-load relation between the action potential approaching the soma and the electrical load of the soma together with the attached dendrites.
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HENDERSON, DORI, and ROBERT F. MILLER. "Evidence for low-voltage-activated (LVA) calcium currents in the dendrites of tiger salamander retinal ganglion cells." Visual Neuroscience 20, no. 2 (March 2003): 141–52. http://dx.doi.org/10.1017/s0952523803202054.
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We have evaluated the spatial distribution of low-voltage-activated calcium currents in ganglion cells of the tiger salamander retina. Whole-cell recordings were obtained from ganglion cells in a retinal slice preparation and from acutely dissociated ganglion cells that were identified through retrograde dye injection. In single dissociated cells, we estimated the magnitude (pA) and current density (pA/pF) of LVA currents in ganglion cells, both with and without dendritic processes. Ganglion cells that retained a portion of their dendritic arbor had larger LVA calcium currents and higher LVA current densities than those which lacked processes. When cell capacitance measurements were used to derive the surface area of the soma and dendritic processes, we concluded that a higher LVA current density was present in the dendrites; we estimate that, on average, the current density in the dendrites is approximately five times that of the soma. The presence of a significant density of LVA calcium channels in the dendrites of ganglion cells suggests that they could be involved in a number of cellular functions, including dendritic integration of synaptic currents, impulse generation, and homeostatic functions related to changes in the intradendritic calcium concentration.
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Bastian, Joseph, and Jerry Nguyenkim. "Dendritic Modulation of Burst-Like Firing in Sensory Neurons." Journal of Neurophysiology 85, no. 1 (January 1, 2001): 10–22. http://dx.doi.org/10.1152/jn.2001.85.1.10.
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This report describes the variability of spontaneous firing characteristics of sensory neurons, electrosensory lateral line lobe (ELL) pyramidal cells, within the electrosensory lateral line lobe of weakly electric fish in vivo. We show that these cells' spontaneous firing frequency, measures of spike train regularity (interspike interval coefficient of variation), and the tendency of these cells to produce bursts of action potentials are correlated with the size of the cell's apical dendritic arbor. We also show that bursting behavior may be influenced or controlled by descending inputs from higher centers that provide excitatory and inhibitory inputs to the pyramidal cells' apical dendrites. Pyramidal cells were classified as “bursty” or “nonbursty” according to whether or not spike trains deviated significantly from the expected properties of random (Poisson) spike trains of the same average firing frequency, and, in the case of bursty cells, the maximum within-burst interspike interval characteristic of bursts was determined. Each cell's probability of producing bursts above the level expected for a Poisson spike train was determined and related to spontaneous firing frequency and dendritic morphology. Pyramidal cells with large apical dendritic arbors have lower rates of spontaneous activity and higher probabilities of producing bursts above the expected level, while cells with smaller apical dendrites fire at higher frequencies and are less bursty. The effect of blocking non- N-methyl-d-aspartate (non-NMDA) glutamatergic synaptic inputs to the apical dendrites of these cells, and to local inhibitory interneurons, significantly reduced the spontaneous occurrence of spike bursts and intracellular injection of hyperpolarizing current mimicked this effect. The results suggest that bursty firing of ELL pyramidal cells may be under descending control allowing activity in electrosensory feedback pathways to influence the firing properties of sensory neurons early in the processing hierarchy.
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Buzsáki, György, and Adam Kandel. "Somadendritic Backpropagation of Action Potentials in Cortical Pyramidal Cells of the Awake Rat." Journal of Neurophysiology 79, no. 3 (March 1, 1998): 1587–91. http://dx.doi.org/10.1152/jn.1998.79.3.1587.
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Buzsáki, György and Adam Kandel. Somadendritic backpropagation of action potentials in cortical pyramidal cells of the awake rat. J. Neurophysiol. 79: 1587–1591, 1998. The invasion of fast (Na+) spikes from the soma into dendrites was studied in single pyramidal cells of the sensorimotor cortex by simultaneous extracellular recordings of the somatic and dendritic action potentials in freely behaving rats. Field potentials and unit activity were monitored with multiple-site silicon probes along trajectories perpendicular to the cortical layers at spatial intervals of 100 μm. Dendritic action potentials of individual layer V pyramidal neurons could be recorded up to 400 μm from the cell body. Action potentials were initiated at the somatic recording site and traveled back to the apical dendrite at a velocity of 0.67 m/s. Current source density analysis of the action potential revealed time shifted dipoles, supporting the view of active spike propagation in dendrites. The presented method is suitable for exploring the conditions affecting the somadendritic propagation action of potentials in the behaving animal.
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Kato, Mizuki, and Erik De Schutter. "Models of Purkinje cell dendritic tree selection during early cerebellar development." PLOS Computational Biology 19, no. 7 (July 24, 2023): e1011320. http://dx.doi.org/10.1371/journal.pcbi.1011320.
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We investigate the relationship between primary dendrite selection of Purkinje cells and migration of their presynaptic partner granule cells during early cerebellar development. During postnatal development, each Purkinje cell grows more than three dendritic trees, from which a primary tree is selected for development, whereas the others completely retract. Experimental studies suggest that this selection process is coordinated by physical and synaptic interactions with granule cells, which undergo a massive migration at the same time. However, technical limitations hinder continuous experimental observation of multiple cell populations. To explore possible mechanisms underlying this selection process, we constructed a computational model using a new computational framework, NeuroDevSim. The study presents the first computational model that simultaneously simulates Purkinje cell growth and the dynamics of granule cell migrations during the first two postnatal weeks, allowing exploration of the role of physical and synaptic interactions upon dendritic selection. The model suggests that interaction with parallel fibers is important to establish the distinct planar morphology of Purkinje cell dendrites. Specific rules to select which dendritic trees to keep or retract result in larger winner trees with more synaptic contacts than using random selection. A rule based on afferent synaptic activity was less effective than rules based on dendritic size or numbers of synapses.
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Elmquist, Lennart, Attila Diószegi, and Peter Svidró. "Influence of Primary Austenite on the Nucleation of Eutectic Cells." Key Engineering Materials 457 (December 2010): 61–66. http://dx.doi.org/10.4028/www.scientific.net/kem.457.61.
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The solidification of gray cast iron starts with the precipitation of primary austenite. This phase nucleates either as columnar or equiaxed dendrites depending on whether nucleation occurs on the mould wall or on particles and impurities in the melt. In this work, the nucleation of primary austenite and its influence on the eutectic solidification has been investigated using different amounts of iron powder as inoculants. Besides, the influence of different cooling rates was also examined. Within each austenite grain there is a microstructure, and this microstructure was investigated using a color etching technique to reveal the eutectic cells and the dendritic network. It is shown how the cooling rate affects the dendritic network and the secondary dendrite arm spacing, and how the microstructure can be related to the macrostructure through dendrite arm spacing. The secondary dendrite arm spacing is a quantification of the primary austenite belonging to the primary solidification, and it will be shown how the eutectic cell size is related to the secondary dendrite arm spacing. The total amount of oxygen influences the microstructural dimensions. This effect, on the other hand, is influenced by the cooling rate. The number of eutectic cells versus eutectic cell size show two distinct behaviors depending on whether being inoculated with iron powder or a mixture of iron powder and commercial inoculant. The addition of a commercial inoculant decreases eutectic cell size and increases the number of cells, while iron powder almost only changes cell size.
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Morishita, Wade, and Bradley E. Alger. "Direct Depolarization and Antidromic Action Potentials Transiently Suppress Dendritic IPSPs in Hippocampal CA1 Pyramidal Cells." Journal of Neurophysiology 85, no. 1 (January 1, 2001): 480–84. http://dx.doi.org/10.1152/jn.2001.85.1.480.
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Whole-cell current-clamp recordings were made from distal dendrites of rat hippocampal CA1 pyramidal cells. Following depolarization of the dendritic membrane by direct injection of current pulses or by back-propagating action potentials elicited by antidromic stimulation, evoked γ-aminobutyric acid-A (GABAA) receptor-mediated inhibitory postsynaptic potentials (IPSPs) were transiently suppressed. This suppression had properties similar to depolarization-induced suppression of inhibition (DSI): it was enhanced by carbachol, blocked by dendritic hyperpolarization sufficient to prevent action potential invasion, and reduced by 4-aminopyridine (4-AP) application. Thus DSI or a DSI-like process can be recorded in CA1 distal dendrites. Moreover, localized application of TTX to stratum pyramidale blocked somatic action potentials and somatic IPSPs, but not dendritic IPSPs or DSI induced by direct dendritic depolarization, suggesting DSI is expressed in part in the dendrites. These data extend the potential physiological roles of DSI.
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Leonard, Carrie E., Maryna Baydyuk, Marissa A. Stepler, Denver A. Burton, and Maria J. Donoghue. "EphA7 isoforms differentially regulate cortical dendrite development." PLOS ONE 15, no. 12 (December 4, 2020): e0231561. http://dx.doi.org/10.1371/journal.pone.0231561.
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The shape of a neuron facilitates its functionality within neural circuits. Dendrites integrate incoming signals from axons, receiving excitatory input onto small protrusions called dendritic spines. Therefore, understanding dendritic growth and development is fundamental for discerning neural function. We previously demonstrated that EphA7 receptor signaling during cortical development impacts dendrites in two ways: EphA7 restricts dendritic growth early and promotes dendritic spine formation later. Here, the molecular basis for this shift in EphA7 function is defined. Expression analyses reveal that EphA7 full-length (EphA7-FL) and truncated (EphA7-T1; lacking kinase domain) isoforms are dynamically expressed in the developing cortex. Peak expression of EphA7-FL overlaps with dendritic elaboration around birth, while highest expression of EphA7-T1 coincides with dendritic spine formation in early postnatal life. Overexpression studies in cultured neurons demonstrate that EphA7-FL inhibits both dendritic growth and spine formation, while EphA7-T1 increases spine density. Furthermore, signaling downstream of EphA7 shifts during development, such that in vivo inhibition of mTOR by rapamycin in EphA7-mutant neurons ameliorates dendritic branching, but not dendritic spine phenotypes. Finally, direct interaction between EphA7-FL and EphA7-T1 is demonstrated in cultured cells, which results in reduction of EphA7-FL phosphorylation. In cortex, both isoforms are colocalized to synaptic fractions and both transcripts are expressed together within individual neurons, supporting a model where EphA7-T1 modulates EphA7-FL repulsive signaling during development. Thus, the divergent functions of EphA7 during cortical dendrite development are explained by the presence of two variants of the receptor.
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Golding, Nace L., William L. Kath, and Nelson Spruston. "Dichotomy of Action-Potential Backpropagation in CA1 Pyramidal Neuron Dendrites." Journal of Neurophysiology 86, no. 6 (December 1, 2001): 2998–3010. http://dx.doi.org/10.1152/jn.2001.86.6.2998.
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In hippocampal CA1 pyramidal neurons, action potentials are typically initiated in the axon and backpropagate into the dendrites, shaping the integration of synaptic activity and influencing the induction of synaptic plasticity. Despite previous reports describing action-potential propagation in the proximal apical dendrites, the extent to which action potentials invade the distal dendrites of CA1 pyramidal neurons remains controversial. Using paired somatic and dendritic whole cell recordings, we find that in the dendrites proximal to 280 μm from the soma, single backpropagating action potentials exhibit <50% attenuation from their amplitude in the soma. However, in dendritic recordings distal to 300 μm from the soma, action potentials in most cells backpropagated either strongly (26–42% attenuation; n = 9/20) or weakly (71–87% attenuation; n = 10/20) with only one cell exhibiting an intermediate value (45% attenuation). In experiments combining dual somatic and dendritic whole cell recordings with calcium imaging, the amount of calcium influx triggered by backpropagating action potentials was correlated with the extent of action-potential invasion of the distal dendrites. Quantitative morphometric analyses revealed that the dichotomy in action-potential backpropagation occurred in the presence of only subtle differences in either the diameter of the primary apical dendrite or branching pattern. In addition, action-potential backpropagation was not dependent on a number of electrophysiological parameters (input resistance, resting potential, voltage sensitivity of dendritic spike amplitude). There was, however, a striking correlation of the shape of the action potential at the soma with its amplitude in the dendrite; larger, faster-rising, and narrower somatic action potentials exhibited more attenuation in the distal dendrites (300–410 μm from the soma). Simple compartmental models of CA1 pyramidal neurons revealed that a dichotomy in action-potential backpropagation could be generated in response to subtle manipulations of the distribution of either sodium or potassium channels in the dendrites. Backpropagation efficacy could also be influenced by local alterations in dendritic side branches, but these effects were highly sensitive to model parameters. Based on these findings, we hypothesize that the observed dichotomy in dendritic action-potential amplitude is conferred primarily by differences in the distribution, density, or modulatory state of voltage-gated channels along the somatodendritic axis.
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Cabeza-Cabrerizo, Mar, Ana Cardoso, Carlos M. Minutti, Mariana Pereira da Costa, and Caetano Reis e Sousa. "Dendritic Cells Revisited." Annual Review of Immunology 39, no. 1 (April 26, 2021): 131–66. http://dx.doi.org/10.1146/annurev-immunol-061020-053707.
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Dendritic cells (DCs) possess the ability to integrate information about their environment and communicate it to other leukocytes, shaping adaptive and innate immunity. Over the years, a variety of cell types have been called DCs on the basis of phenotypic and functional attributes. Here, we refocus attention on conventional DCs (cDCs), a discrete cell lineage by ontogenetic and gene expression criteria that best corresponds to the cells originally described in the 1970s. We summarize current knowledge of mouse and human cDC subsets and describe their hematopoietic development and their phenotypic and functional attributes. We hope that our effort to review the basic features of cDC biology and distinguish cDCs from related cell types brings to the fore the remarkable properties of this cell type while shedding some light on the seemingly inordinate complexity of the DC field.
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Carneiro, Sueli Coelho, Raphael Medeiros, Marcelo Alves Brollo, Marcia Ramos-e-Silva, and Mirian Nacagami Sotto. "Dendritic skin cells." Expert Review of Dermatology 3, no. 4 (August 2008): 509–15. http://dx.doi.org/10.1586/17469872.3.4.509.
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Takeuchi, Satoshi, and Masutaka Furue. "Dendritic Cells—Ontogeny—." Allergology International 56, no. 3 (2007): 215–23. http://dx.doi.org/10.2332/allergolint.r-07-149.
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Vermaelen, Karim, and Romain Pauwels. "Pulmonary Dendritic Cells." American Journal of Respiratory and Critical Care Medicine 172, no. 5 (September 2005): 530–51. http://dx.doi.org/10.1164/rccm.200410-1384so.
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Beriou, Gaelle, Aurelie Moreau, and Maria C. Cuturi. "Tolerogenic dendritic cells." Current Opinion in Organ Transplantation 17, no. 1 (February 2012): 42–47. http://dx.doi.org/10.1097/mot.0b013e32834ee662.
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KABEL, P. J., H. A. M. VOORBIJ, M. DE HAAN, R. D. VAN DER GAAG, and H. A. DREXHAGE. "Intrathyroidal Dendritic Cells*." Journal of Clinical Endocrinology & Metabolism 66, no. 1 (January 1988): 199–207. http://dx.doi.org/10.1210/jcem-66-1-199.
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Jegalian, Armin G., Fabio Facchetti, and Elaine S. Jaffe. "Plasmacytoid Dendritic Cells." Advances in Anatomic Pathology 16, no. 6 (November 2009): 392–404. http://dx.doi.org/10.1097/pap.0b013e3181bb6bc2.
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Schiavi, Elisa, Sylwia Smolinska, and Liam O’Mahony. "Intestinal dendritic cells." Current Opinion in Gastroenterology 31, no. 2 (March 2015): 98–103. http://dx.doi.org/10.1097/mog.0000000000000155.
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Ovali, E. "Dendritic cells therapy." ISBT Science Series 2, no. 2 (November 2007): 130–34. http://dx.doi.org/10.1111/j.1751-2824.2007.00128.x.
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Petty, Ross E., and David W. C. Hunt. "Neonatal dendritic cells." Vaccine 16, no. 14-15 (August 1998): 1378–82. http://dx.doi.org/10.1016/s0264-410x(98)00095-4.
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Valladeau, Jenny, and Sem Saeland. "Cutaneous dendritic cells." Seminars in Immunology 17, no. 4 (August 2005): 273–83. http://dx.doi.org/10.1016/j.smim.2005.05.009.
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Reis e Sousa, Caetano. "Harnessing dendritic cells." Seminars in Immunology 23, no. 1 (February 2011): 1. http://dx.doi.org/10.1016/j.smim.2011.02.003.
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Collin, Matthew, and Florent Ginhoux. "Human dendritic cells." Seminars in Cell & Developmental Biology 86 (February 2019): 1–2. http://dx.doi.org/10.1016/j.semcdb.2018.04.015.
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Ardavi´n, Carlos. "Thymic dendritic cells." Immunology Today 18, no. 7 (July 1997): 350–61. http://dx.doi.org/10.1016/s0167-5699(97)01090-6.
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Kindler, Vincent, and Jean-François Arrighi. "Dendritic cells unveiled." Trends in Immunology 23, no. 2 (February 2002): 110. http://dx.doi.org/10.1016/s1471-4906(01)02093-2.
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