Relevant bibliographies by topics / Immature and mature dendritic cells

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  2. Dissertations / Theses
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Academic literature on the topic 'Immature and mature dendritic cells'

Author: Grafiati
Published: 18 May 2024

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Journal articles on the topic "Immature and mature dendritic cells"

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Cao, Yun, Ingrid K. Bender, Athanasios K. Konstantinidis, Soon Cheon Shin, Christine M. Jewell, John A. Cidlowski, Robert P. Schleimer, and Nick Z. Lu. "Glucocorticoid receptor translational isoforms underlie maturational stage-specific glucocorticoid sensitivities of dendritic cells in mice and humans." Blood 121, no. 9 (February 28, 2013): 1553–62. http://dx.doi.org/10.1182/blood-2012-05-432336.

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Key Points Mature, but not immature, dendritic cells are sensitive to glucocorticoid-induced apoptosis. Mature, but not immature, dendritic cells express proapoptotic glucocorticoid receptor translational isoforms.
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Xin, Hai-ming, Yi-zhi Peng, Zhi-qiang Yuan, and Hao Guo. "In vitro maturation and migration of immature dendritic cells after chemokine receptor 7 transfection." Canadian Journal of Microbiology 55, no. 7 (July 2009): 859–66. http://dx.doi.org/10.1139/w09-041.

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Dendritic cells are specialized antigen-presenting cells that regulate immunity and tolerance. Chemokine receptor 7 (CCR7), which is expressed by mature dendritic cells, mediates the migration of the cells to secondary lymphoid organs and thus regulates immune responses. It has been demonstrated that immature dendritic cells can induce immune tolerance, but they do not express CCR7 and cannot migrate to secondary lymphoid organs. We transfected immature dendritic cells with a recombinant adenovirus carrying the CCR7 gene to obtain immature dendritic cells with the ability to migrate. The maturity of the cells was monitored by scanning electron microscopy and flow cytometry. In addition, we assessed the ability of cells to migrate and the function of the cells using in vitro chemotactic and mixed leukocyte reaction assays. The results showed that immature dendritic cells became semi-mature, exhibiting a mild upregulation of co-stimulatory molecular expression and a few dendritic processes. Immunofluorescence assay and Western blotting indicated that CCR7 protein expression increased significantly in immature dendritic cells following CCR7 gene transfection. The in vitro chemotactic assay showed a significantly enhanced ability to migrate in response to CCL19 following CCR7 gene transfection. Moreover, transfected cells showed an enhanced ability to stimulate allogeneic T cell proliferation in vitro, but their ability was significantly weaker than that of mature dendritic cells. Interleukin-10 inhibited the differentiation and maturation of immature dendritic cells. It is concluded that, following CCR7 gene transfection, immature dendritic cells exhibit an enhanced ability to migrate and some of the characteristics of mature cells. Thus, these cells are of potential clinical significance in studies of immune tolerance induction during skin grafting after severe burns.
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Bell, Diana, Pascale Chomarat, Denise Broyles, George Netto, Ghada Moumneh Harb, Serge Lebecque, Jenny Valladeau, Jean Davoust, Karolina A. Palucka, and Jacques Banchereau. "In Breast Carcinoma Tissue, Immature Dendritic Cells Reside within the Tumor, Whereas Mature Dendritic Cells Are Located in Peritumoral Areas." Journal of Experimental Medicine 190, no. 10 (November 15, 1999): 1417–26. http://dx.doi.org/10.1084/jem.190.10.1417.

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We have analyzed the presence of immature and mature dendritic cells (DCs) within adenocarcinoma of the breast using immunohistochemistry. Immature DCs were defined by expression of CD1a-, Langerin-, and intracellular major histocompatibility complex class II–rich vesicles. Mature DCs were defined by expression of CD83 and DC-Lamp. Breast carcinoma cells were defined by morphology and/or cytokeratin expression. We demonstrate two levels of heterogeneity of DCs infiltrating breast carcinoma tissue: (a) immature CD1a+ DCs, mostly of the Langerhans cell type (Langerin+), were retained within the tumor bed in 32/32 samples and (b) mature DCs, CD83+DC-Lamp+, present in 20/32 samples, are confined to peritumoral areas. The high numbers of immature DCs found in the tumor may be best explained by high levels of macrophage inflammatory protein 3α expression by virtually all tumor cells. Confirming the immature/mature DC compartmentalization pattern, in vitro–generated immature DCs adhere to the tumor cells, whereas mature DCs adhere selectively to peritumoral areas. In some cases, T cells are clustering around the mature DCs in peritumoral areas, thus resembling the DC–T cell clusters of secondary lymphoid organs, which are characteristic of ongoing immune reactions.
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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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Cavrois, Marielle, Jason Neidleman, Jason F. Kreisberg, David Fenard, Christian Callebaut, and Warner C. Greene. "Human Immunodeficiency Virus Fusion to Dendritic Cells Declines as Cells Mature." Journal of Virology 80, no. 4 (February 15, 2006): 1992–99. http://dx.doi.org/10.1128/jvi.80.4.1992-1999.2006.

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ABSTRACT The maturation of dendritic cells (DCs) is associated with a diminished ability to support human immunodeficiency virus (HIV) replication; however, the precise step in the HIV life cycle impaired by DC maturation remains uncertain. Using an HIV virion-based fusion assay, we now show that HIV fusion to monocyte-derived DCs (MDDCs) both decreases and kinetically slows when DCs are induced to mature with poly(I:C) and tumor necrosis factor alpha. Specifically, laboratory-adapted CCR5-tropic 81A virions fused with markedly lower efficiency to mature MDDCs than immature DCs. In contrast, fusion of NL4-3, the isogenic CXCR4-tropic counterpart of 81A, was low in both immature and mature MDDCs. Fusion mediated by primary HIV envelopes, including seven CCR5- and four CXCR4-tropic envelopes, also decreased with DC maturation. The kinetics of virion fusion were also altered by both the state of DC maturation and the coreceptor utilized. Fusion of 81A and NL4-3 virions was delayed in mature compared to immature MDDCs, and NL4-3 fused more slowly than 81A in both mature and immature MDDCs. Surprisingly, primary envelopes with CXCR4 tropism mediated fusion to immature MDDCs with efficiencies similar to those of primary CCR5-tropic envelopes. This result contrasted with the marked preferential fusion of the laboratory-adapted 81A over NL4-3 in immature MDDCs and in ex vivo Langerhans cells, indicating that these laboratory-adapted HIV strains do not fully recapitulate all of the properties of primary HIV isolates. In conclusion, our results demonstrate that the defect in HIV replication observed in mature MDDCs stems at least in part from a decline in viral fusion.
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Hipolito, Jolly, Hagit Peretz-Soroka, Manli Zhang, Ke Yang, Soheila Karimi-Abdolrezaee, Francis Lin, and Sam Kung. "A New Microfluidic Platform for Studying Natural Killer Cell and Dendritic Cell Interactions." Micromachines 10, no. 12 (December 5, 2019): 851. http://dx.doi.org/10.3390/mi10120851.

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The importance of the bi-directional natural killer–dendritic cell crosstalk in coordinating anti-tumour and anti-microbial responses in vivo has been well established. However, physical parameters associated with natural killer–dendritic cell interactions have not been fully elucidated. We have previously used a simple “Y” shaped microfluidic device to study natural killer cell-migratory responses toward chemical gradients from a conditioned medium of dendritic cells. There are, however, limitations of the Y-shaped microfluidic devices that could not support higher throughput analyses and studies of cell–cell interactions. Here, we report two novel microfluidic devices (D3-Chip, T2-Chip) we applied in advanced studies of natural killer-cell migrations and their interactions with dendritic cells in vitro. The D3-Chip is an improved version of the previously published Y-shaped device that supports high-throughput analyses and docking of the cells of interest in the migration assay before they are exposed to a chemical gradient. The T2-Chip is created to support analyses of natural killer–dendritic cell cell–cell interactions without the requirement of promoting a natural killer cell to migrate long distances to find a loaded dendritic cell in the device. Using these two microfluidic platforms, we observe quantitative differences in the abilities of the immature and lipopolysaccharide-activated mature dendritic cells to interact with activated natural killer cells. The contact time between the activated natural killer cells and immature dendritic cells is significantly longer than that of the mature dendritic cells. There is a significantly higher frequency of an immature dendritic cell coming into contact with multiple natural killer cells and/or making multiple simultaneous contacts with multiple natural killer cells. To contrast, an activated natural killer cell has a significantly higher frequency of coming into contact with the mature dendritic cells than immature dendritic cells. Collectively, these differences in natural killer–dendritic cell interactions may underlie the differential maturation of immature dendritic cells by activated natural killer cells. Further applications of these microfluidic devices in studying natural killer–dendritic cell crosstalk under defined microenvironments shall enrich our understanding of the functional regulations of natural killer cells and dendritic cells in the natural killer–dendritic cell crosstalk.
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Ogasawara, Masahiro, Junji Tanaka, Masahiro Imamura, and Masaharu Kasai. "CCL19 and CCL21 Chemokines Induce Endocytosis and Augment Antigen Presentation in Human Mature Dendritic Cells." Blood 104, no. 11 (November 16, 2004): 2651. http://dx.doi.org/10.1182/blood.v104.11.2651.2651.

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Abstract Dendritic cells (DCs) are potent antigen presenting cells capable of regulating immune responses. DCs lose the ability to capture and process antigens during maturation. In the present study, we examined the effects of CCR7 ligands, CCL19 and CCL21, on endocytosis and antigen presentation in human mature dendritic cells. Immature DCs were generated from peripheral blood monocytes by culturing with GM-CSF and IL4 for 2–3 days. For maturation, immature DCs were cultured with the addition of TNFα, IL1β, IL6 and prostaglandin E2 for another 24 hours. Immature or mature DCs were incubated with FITC-dextran with or without CCL19. Immature DCs internalized FITC-dextran efficiently independent of the presence of CCL19 after 1 hour incubation. On the other hand, mature DCs scarcely internalized FITC-dextran without CCL19. In the presence of CCL19, however, mature DCs internalized FITC-dextran significantly (approximately 60% positive). The effect of CCL19 on the uptake of FITC-dextran in mature DCs was dose and time dependent. CCL21 exerted a similar effect on mature DCs. Next, we examined whether CCL19 facilitates antigen presentation in mature dendritic cells. CD4+ T cells were cultured with irradiated autologous mature DCs which had been incubated with leukemia cell lysate with or without CCL19. Marked proliferation of CD4+ T cells occurred only when these cells were cultured with mature DCs loaded with leukemia cell lysate in the presence of CCL19. This is the first demonstration that chemokines have a pivotal role in endocytosis and antigen presentation by human monocyte-derived dendritic cells to the best of our knowledge. These results demonstrated that generation of potent antigen-loaded mature DCs in relatively short term culture using various cytokines and chemokines may have an important clinical implication to facilitate DC-based immunotherapy.
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Gerosa, Franca, Barbara Baldani-Guerra, Carla Nisii, Viviana Marchesini, Giuseppe Carra, and Giorgio Trinchieri. "Reciprocal Activating Interaction between Natural Killer Cells and Dendritic Cells." Journal of Experimental Medicine 195, no. 3 (February 4, 2002): 327–33. http://dx.doi.org/10.1084/jem.20010938.

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We analyzed the interaction between human peripheral blood natural killer (NK) cells and monocyte-derived immature dendritic cells (DC). Fresh NK cells were activated, as indicated by the induced expression of the CD69 antigen, and their cytolytic activity was strongly augmented by contact with lipopolysaccharide (LPS)-treated mature DC, or with immature DC in the presence of the maturation stimuli LPS, Mycobacterium tuberculosis or interferon (IFN)-α. Reciprocally, fresh NK cells cultured with immature DC in the presence of the maturation stimuli strongly enhanced DC maturation and interleukin (IL)-12 production. IL-2–activated NK cells directly induced maturation of DC and enhanced their ability to stimulate allogeneic naive CD4+ T cells. The effects of NK cells were cell contact dependent, although the secretion of IFN-γ and TNF also contributed to DC maturation. Within peripheral blood lymphocytes the reciprocal activating interaction with DC was restricted to NK cells, because the other lymphocyte subsets were neither induced to express CD69, nor induced to mature in contact with DC. These data demonstrated for the first time a bidirectional cross talk between NK cells and DC, in which NK cells activated by IL-2 or by mature DC induce DC maturation.
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Roche, Paul A., Satoshi Ishido, Laurence C. Eisenlohr, and Kyung-Jin Cho. "Activation of Dendritic Cells Alters the Mechanism of MHC Class II Antigen Presentation to CD4 T Cells." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 140.14. http://dx.doi.org/10.4049/jimmunol.204.supp.140.14.

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Abstract Both immature and mature DCs can process and present foreign antigens to CD4 T cells, however the mechanism by which MHC-II in mature DCs acquires antigenic peptides remains unknown. To address this we have studied antigen processing and presentation of two distinct CD4 T cells epitopes of the influenza virus haemagglutinin coat protein by both immature and mature DCs. We find that immature DCs almost exclusively use newly-synthesized MHC-II targeted to DM+ late endosomes for presentation to influenza virus-specific CD4 T cells. By contrast, mature DCs exclusively use recycling MHC-II that traffics to both early and late endosomes for antigenic peptide binding. Knock-down of the small GTPase Rab11a partially inhibits recycling of MHC-II in mature DCs and inhibits presentation of an influenza virus hemagglutinin CD4 T cell epitope generated in early endosomes. By contrast, knock-down of Rab11a does not affect presentation of an influenza virus hemagglutinin CD4 T cell epitope that is DM-dependent and is generated in late endosomes in both immature and mature DCs. These studies highlight a “division of labor” in MHC-II peptide binding in which immature DCs preferentially present antigens acquired in Rab11a− DM+ late endosomes whereas mature DCs use recycling MHC-II to present antigenic peptides acquired in both Rab11a+ early endosomes and Rab11a− endosomes for CD4 T cell activation.
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Koch, F., B. Trockenbacher, E. Kämpgen, O. Grauer, H. Stössel, A. M. Livingstone, G. Schuler, and N. Romani. "Antigen processing in populations of mature murine dendritic cells is caused by subsets of incompletely matured cells." Journal of Immunology 155, no. 1 (July 1, 1995): 93–100. http://dx.doi.org/10.4049/jimmunol.155.1.93.

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Abstract Immature dendritic cells (DC), such as freshly isolated Langerhans cells (LC), are excellent at processing native protein Ag. During short term culture they shut off MHC class II synthesis and down-regulate their processing capacity. They retain, however, the MHC/peptide complexes, up-regulate adhesion and costimulatory molecules, and acquire the ability to sensitize T cells. Two reports describing substantial processing activity in populations of mature DC prompted us to undertake an extensive comparative study of the Ag-processing capacities of immature vs mature DC. We used a panel of 17 peptide-specific T cell hybridomas restricted by six different MHC class II molecules: I-Ab, I-A(d), I-E(d), hybrid I-A beta dE alpha, I-Ak, and I-Ek. Side by side comparisons revealed in all cases that freshly isolated LC were superior to cultured mature LC in their ability to process native proteins. With some hybridomas, however, we found a considerable degree of processing by populations of cultured LC at high doses of Ag or Ag-presenting cells. This activity, however, did not correlate with the MHC haplotype. Direct comparison over wide ranges of DC doses or Ag doses showed that it was always less than that of corresponding fresh immature LC. Immunoperoxidase staining of cytospins and flow cytometry with mAb In1 disclosed a small (20% maximum) subset of cultured LC expressing the MHC class II-associated invariant chain, indicating ongoing biosynthesis of this molecule and, thus, incomplete maturation of these LC. Therefore, the residual processing activity observed in populations of mature DC may be explained by small subpopulations of incompletely matured DC.
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Dissertations / Theses on the topic "Immature and mature dendritic cells"

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Patel, Ekta. "IgM antibodies enhance the phagocytosis of apoptotic cells by immature dendritic cells." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1462525.

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Thesis (M.S.)--University of California, San Diego, 2009.
Title from first page of PDF file (viewed May 8, 2009). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 45-47).
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Blair, Derek. "Signalling mechanisms regulating proliferation and apoptosis in immature and mature B cells." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400789.

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Geng, Shuo. "Discovery of a New Dendritic Cell Subset Derived from Immature Granulocytes." University of Toledo Health Science Campus / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=mco1294155495.

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Ismail, Ida Shazrina Binti. "Identification of peptides capable of targeting immature dendritic cells using phage display." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/10484.

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The ability of dendritic cells (DC) to be either tolerogenic or immunogenic offers many opportunities to manipulate DC function and genetically modify DC to promote allograft acceptance. However, the greatest challenge in DC gene therapy is the difficulty of achieving successful transfection. At present, DC-targeting gene delivery strategies are hindered by the lack of DC-specific target molecules. Therefore, the essential aim of this study is to isolate and identify peptides capable of targeting immature DC (iDC), in particular those that internalise well as they are likely to be more effective in gene delivery. Phage library of short cyclic peptides expressed on pIII protein of M13 filamentous phage was used first in selection against streptavidin. Phage bearing HPQ and HPM motifs were successfully isolated indicating the feasibility of the library in selecting streptavidin-binding peptides through specific biotin interaction. In order to develop a method for in vitro selection on cell surfaces, the library was used against a cell line expressing αVβ3 integrin. One phage clone with encoded sequence of CLSSPALLC bound to the cell surface and was taken up by the cells expressing the αVβ3 integrin. Using methods established in the previous panning, the library was panned against iDC, after two subtractive pannings against PBMC and CD14+ cells. The phage isolated were characterised by using several methods including flow cytometric analysis and confocal microscopy. Two phage selected, DC4.25 and DC4.44 with encoded peptide sequences of CFPPTFPAC and CTPLLSPFC, respectively, have demonstrated the ability to bind to, and be internalised by, iDC. Soluble biotinylated peptides, which contain the encoded peptide sequences, were synthesised along with sequence-scrambled control peptides. Flow cytometric analysis detected non-specific binding of the monomeric peptides to iDC when used at high concentration. In an attempt to increase the binding avidity of the peptides to iDC, Streptavidin conjugated with Alexa-488® flurophore was used to form complexes with the peptides. However, flow cytometric analysis revealed that the complexes also bound non-specifically to iDC, as binding was also seen in control peptides. Streptavidin conjugated with HRP was then used to form complexes with the peptides, in order to increase the sensitivity of the binding assay. The results corroborated the previous findings, which showed that the peptides bound iDC non-specifically. The failure of the synthetic peptides to bind to iDC might be due to a number of reasons, including loss of cyclised conformation of the peptides during synthesis and insufficient incorporation of sequences that is essential and accountable for the binding, in the synthetic peptides. However, this approach does offer the possibility of identifying cell binding peptides that may allow delivery of genes and other therapeutic or imaging agents.
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Khanolkar, Rahul Chaitanya. "Molecular analysis of ABIN1 expression and immunosuppressive function in immature myeloid cells." Thesis, University of Aberdeen, 2013. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=202767.

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The leukocyte immunoglobulin like receptors (LILRs) are a group of receptors with immunomodulatory effects. Group 1 LILRs comprise of LILRB1, among others, and bind to class 1 MHC molecules and transmits inhibitory signals. Studies have shown that LILRB1 ligation during the monocyte differentiation process into dendritic cells (DCs) results in the generation of a population of cells that are tolerogenic. Here we hypothesize that this tolerogenic nature of the resultant cells is due to the high expression of nuclear factor kappa – light chain enhancer of activated B cells (NF-κB) inhibitor – A20 binding inhibitor of NF-κB signalling 1 (ABIN1). In this study we analyzed the effect that ABIN1 exerts on the maturation of DCs and CD14+HLA-DRlow/- monocytes - a population of cells that have been recently been identified as myeloid derived suppressor cells (MDSCs) in humans. LILRB1 ligated DCs and CD14+HLA-DRlow/- monocytes, when treated with ABIN1 siRNA, displayed an increase in the expression of antigen presentation and co-stimulatory molecules such as CD80, CD86, HLA-DR and HLA-ABC and displayed a greater capacity to produce cytokines like IL-12 and IFN-α. Additionally, they displayed a greater capacity to stimulate the adaptive component of the immune system in terms of IFN-γ production, cell proliferation and adapter molecule and mitogen activated protein kinase (MAPK) activation in T cells. Based on the results we obtained, it can be concluded that ABIN1 plays a significant role in maintaining the immature and suppressive phenotype of immature myeloid cells (IMCs) by dampening NF-κB signalling, while also exerting a negative effect on antiviral signalling.
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Solanes, Paola. "IP3 Receptor 3 controls migration persistency and environment patrolling by immature dendritic cells." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T020/document.

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Le succès de la réponse immunitaire repose en grande partie sur la capacité des leucocytes à se déplacer et à accomplir leur fonction au sein de structures anatomiques précises. Le fait qu’il puisse exister des mécanismes intrinsèques de coordination entre ces fonctions spécifiques et la migration de ces cellules n’a jamais été étudié auparavant. Nos travaux mettent en évidence, pour la première fois, l’existence d’un couplage entre la migration et la macropinocytose dans les cellules dendritiques qui explorent leur environnement en internalisant une grande quantité de matériel extra-cellulaire. C’est la Chaîne Invariante, protéine chaperon impliquée dans l’apprêtement des antigènes, qui est responsable de ce couplage en détournant le moteur Myosine II de l’arrière de la cellule, où elle promeut la migration, vers l’avant de la cellule. Ce recrutement transitoire de Myosin II autour des macropinosomes à l’avant favorise la macropinocytose et la délivrance de l’antigène dans les lysosomes, mais ralentit la cellule. L’implication de la Myosine II à la fois dans la migration et la capture d’antigène permet donc le couplage moléculaire entre ces deux processus et leur coordination spatio-temporelle. Cependant, les voies de signalisation impliquées dans le couplage avant/arrière dans les cellules dendritiques immatures restent encore méconnues. L’ensemble de mes travaux de thèse montrent que la libération de calcium du réticulum endoplasmique à travers les récepteurs IP3 (IP3Rs) est nécessaire pour maintenir le niveau de phosphorylation de la chaîne légère de Myosin (MLC) et la polarisation avant/arrière de Myosine II au cours de la migration des cellules dendritiques immatures. Nous montrons que les récepteurs IP3R1, 2 et 3 sont requis pour atteindre une vitesse maximale en 2- et 3-Dimension, et que le récepteur IP3R3, et dans une moindre mesure IP3R1, favorisent la persistance des cellules. En revanche, l’inhibition de l’expression du récepteur IP3R3 augmente la capacité des cellules dendritiques immatures à capturer l’antigène, ce qui est en accord avec notre résultat montrant que la capture de l'antigène est inversement reliée à la locomotion de cellules dendritiques. Nous proposons que le relargage du calcium par le réticulum endoplasmique favorise l’activité de la myosine II ce qui permet aux cellules dendritiques de ralentir de façon transitoire. Ce relargage calcique permet aux cellules dendritiques du optimiser l'internalisation des antigènes extracellulaires en maintenant leur polarité ce qui leur permet d’optimiser ainsi leur capacité d'échantillonnage de l’environnement
The immune response heavily relies on the migration capacity of leukocytes. These cells must stop in precise anatomical locations to fulfill a particular task. But whether and how specific functions are coordinated with migration by cell-intrinsic mechanisms is not known. We here show that in dendritic cells, which patrol their environment for the presence of antigens by internalizing extracellular material, macropinocytosis is coupled to cell migration. Coupling relies on the diversion of the Myosin II motor from its migratory function at the cell rear to macropinosomes at the cell front by the Invariant Chain, a cell-specific regulator of antigen presentation. Transient Myosin II recruitment at the cell front promotes antigen macropinocytosis and antigen delivery to endolysosomes but antagonizes cell migration. Thus, the requirement for Myosin II for both migration and antigen capture provides a molecular mechanism to couple these two processes and allow their coordination in time and space. However, the signaling pathways involved in back/front coupling in migrating immature DCs remain unknown. Here we show that calcium released from the endoplasmic reticulum through IP3 Receptors (IP3Rs) is required to maintain Myosin regulatory light Chain (MLC) phosphorylation and Myosin II back/front polarization during DC locomotion. We found that while IP3R1, 2 and 3 are required for immature DCs to reach maximal speed in 2-Dimensional and 3-Dimensional environments, IP3R3 and to a lesser extent IP3R1 positively regulate their persistency. On the contrary, silencing of IP3R3 increases antigen uptake by immature DCs, consistent with our finding showing that antigen capture is inversely coupled to DC locomotion (Appendix, manuscript #1). We propose that by promoting myosin II activity, calcium released from the ER help DCs to transiently slow-down to uptake extracellular antigens without losing their polarity and thereby optimizes their environment sampling capacity
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Ito, Takeshi. "Bone marrow endothelial cells induce immature and mature B cell egress in response to erythropoietin." Kyoto University, 2018. http://hdl.handle.net/2433/232127.

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Gutzeit, Cindy. "Interference of Varicella-Zoster Virus (VZV) with the CD1 antigen presenting system on immature dendritic cells." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2009. http://dx.doi.org/10.18452/16059.

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Das human pathogene Varicella-Zoster Virus (VZV) gehört zur Familie der Herpesviren und ist weltweit verbreitet. Die Primärinfektion verursacht Varicellen, welche durch einen bläschenartigen Hautausschlag charakterisiert ist. Im Anschluss daran etabliert VZV eine lebenslange Latenz und verursacht nach Reaktivierung Herpes Zoster. Seit 2004 ist der Lebendimpfstoff aus attenuierten Virionen des VZV-Stammes V-Oka in Deutschland empfohlen. Im Gegensatz zur Infektion mit zirkulierenden virulenten VZV Stämmen tritt nach Verimpfung des Vakzin-Stammes V-Oka kein Exanthem auf. Die Haut ist der Hauptreplikationsort von VZV und immunologische Unterschiede zwischen virulentem VZV und dem Vakzin-Stamm treten hier am deutlichsten auf. In der vorliegenden Arbeit konnte eine neue Immunevasionsstrategie virulenter VZV Stämme aufgedeckt werden, welche erklären könnte, wie virulente VZV Stämme frühe antivirale Immunantworten umgehen. In Hautläsionen von Herpes Zoster Patienten konnte eine massive Infiltration von myeloiden inflammatorischen Dendritischen Zellen beobachtet werden. In vitro Studien mit Monozyten abgeleiteten Dendritischen Zellen (DC), welche inflammatorische DC repräsentieren, zeigten, eine signifikant erhöhte Expression von CD1c Molekülen nach Infektion mit dem Vakzin-Stamm, sowie virulentem VZV. Funktionelle Untersuchungen mit intraepithelialen CD1c-restringierten gamma delta T Zellen zeigten, dass DC nach Infektion mit dem Vakzin-Stamm phänotypisch und funktionell reiften und somit die T Zellen zur IFN-gamma Sekretion stimulierten. Im Gegensatz dazu wurde die funktionelle Reifung von DC, die mit virulentem VZV infiziert waren, geblockt. Folglich wurde kein bioaktives IL-12 sezerniert, welches als entscheidendes Cytokin zum Aufbau einer antiviralen T-Helfer 1 Immunantwort beiträgt. Darüber hinaus konnte gezeigt werden, dass virulentes VZV die Signalkaskade des Toll-like Rezeptors 2 (TLR2) in DC inhibiert und somit die IL-12 Produktion verhindert.
Varicella-zoster virus (VZV) which belongs to the family of herpesviruses is restricted to humans and distributed worldwide. Primary infection of VZV causes chickenpox characterized by a disseminated rash. Thereafter, VZV establishes a lifelong latency and can be reactivated to cause herpes zoster. Since 2004 the attenuated strain V-Oka of VZV was licensed for Germany to immunize children against VZV infection. In contrast to infection by circulating virulent VZV strains, vaccination with V-Oka remains asymptomatic. The skin is the major replication site of VZV and immunological differences between virulent VZV and the vaccine should become most apparent within this immune organ. In summary, this study discovered a new immune evasion strategy of virulent VZV strains which might explain how virulent VZV strains overcome innate antiviral responses. A strong infiltration of myeloid-derived inflammatory DCs has been detected in skin lesions of herpes zoster patients. In vitro studies with monocyte-derived dendritic cells (DCs), reflecting inflammatory DCs, showed that they were efficiently infected by both, the vaccine and a virulent VZV strain. Intriguingly, a significant upregulation of CD1c molecules on VZV-infected DCs was observed. Functional investigations using intraepithelial CD1c-restricted gamma delta T cells revealed that DCs infected with the vaccine virus were fully instructed to mature, thereby promoting IFN-gamma secretion of gamma-delta T cells. In striking contrast, DCs infected with virulent VZV strains were efficiently blocked to mature functionally. In detail, they did not secrete bioactive IL-12 which is an instrumental cytokine for generation of antiviral T helper 1 responses. Moreover, virulent VZV blocked Toll-like receptor 2 (TLR2) signaling in DCs thereby preventing production of bioactive IL-12 which in turn inhibited IFN-gamma secretion by gamma-delta T cells.
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Yu, Hyun Jae. "HIV Traffics Through a Specialized, Surface-accessible Intracellular Compartment During Trans-infection of T Cells by Mature Dendritic Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1266871870.

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Kather, Angela. "Pro- and antiapoptotic events in Herpes simplex virus type 1 (HSV-1) infection of immature dendritic cells." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16464.

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Herpes simplex virus Typ 1 (HSV-1) ist ein humanpathogenes Virus der Familie Herpesviridae. Für eine erfolgreiche Virusreplikation besitzt HSV-1 mehrere Gene, die in den meisten infizierten Zelltypen Apoptose verhindern. Im Gegensatz dazu führt die HSV-1 Infektion eines zentralen Zelltyps des Immunsystems, den unreifen dendritischen Zellen (iDCs), zu Apoptose. Dies könnte ein Aspekt der HSV-1 Immunevasion sein. Bisher waren die Ursachen der Apoptose von HSV-1 infizierten iDCs unzureichend aufgeklärt. Es wurde jedoch gezeigt, dass das antiapoptotische zelluläre Protein c-FLIP in HSV-1 infizierten iDCs reduziert ist. In dieser Arbeit wurde die c-FLIP Menge in iDCs erstmalig mit Hilfe von RNA Interferenz erfolgreich reduziert. Dies bestätigte die Bedeutung von c-FLIP für die Lebensfähigkeit von iDCs. Folglich könnte auch die Reduktion der c-FLIP Menge nach HSV-1 Infektion iDCs für Apoptose empfindlich machen. Die HSV-1 induzierte c-FLIP Reduktion erfolgte in späten Stadien der Infektion, abhängig von der ordnungsgemäßen Expression viraler „early“ und „leaky late“ Gene. Sie fand nicht auf RNA Ebene statt und war unabhängig vom Proteasom und der Bindung an den „death inducing signaling complex“. Stattdessen wurde c-FLIP wahrscheinlich von einer viralen oder zellulären Protease abgebaut. In dieser Arbeit wurde erstmals gezeigt, dass zusätzlich zu Veränderungen im zellulären Apoptosesignalnetzwerk der Mangel an einem antiapoptotischen viralen Faktor zur Apoptose von HSV-1 infizierten iDCs beiträgt. Eine Microarray Analyse der HSV-1 Genexpression ergab, dass HSV-1 Latenz-assoziierte Transkripte (LATs) in apoptotischen iDCs signifikant geringer exprimiert waren als in nicht-apoptotischen epithelialen Zellen. LATs besitzen in Neuronen und epithelialen Zellen eine antiapoptotische Aktivität. Diese könnte den Mangel an c-FLIP kompensieren. Übereinstimmend mit dieser Hypothese induzierte eine HSV-1 LAT-Deletionsmutante mehr Apoptose in iDCs im Vergleich zum Wildtyp-Virus.
Herpes simplex virus type 1 (HSV-1) is a human pathogen which belongs to the family Herpesviridae. HSV-1 encodes several genes, which serve to efficiently prevent apoptosis in most infected cell types, thereby ensuring successful virus replication. In contrast, HSV-1 infection of one central cell type of the immune system, immature dendritic cells (iDCs), results in apoptosis. This could be one aspect of HSV-1 immunevasion. So far, the mechanisms underlying apoptosis of HSV-1 infected iDCs were poorly defined. However, it has been shown that the antiapoptotic cellular protein c-FLIP is reduced in HSV-1 infected iDCs. In this work, the amount of c-FLIP was for the first time successfully reduced in iDCs by RNA interference. This confirmed the importance of c-FLIP for viability of iDCs. Therefore, it is likely that c-FLIP reduction after HSV-1 infection also sensitizes iDCs to apoptosis. HSV-1 induced c-FLIP reduction occurred at late stages of infection and was dependent on proper expression of early and leaky late virus genes. Furthermore, it was not operative at the RNA level and was independent from the proteasome and binding to the death inducing signaling complex. Rather, c-FLIP was presumably degraded by a viral or cellular protease. In this work it was shown for the first time, that in addition to changes in the cellular apoptosis signaling network, the lack of one antiapoptotic viral factor contributes to apoptosis of HSV-1 infected iDCs. HSV-1 latency-associated transcripts (LATs) were significantly lower expressed in apoptotic iDCs compared to non-apoptotic epithelial cells, determined by microarray analysis of HSV-1 gene expression. It is known that in neurons and epithelial cells, LATs possess a potent antiapoptotic activity. This could compensate the lack of c-FLIP. Consistent with this hypothesis, a LAT deletion mutant of HSV-1 induced more apoptosis in iDCs compared to the respective wild type virus.
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Book chapters on the topic "Immature and mature dendritic cells"

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Rolink, A. G., F. Melchers, and J. Andersson. "The Transition from Immature to Mature B Cells." In Current Topics in Microbiology and Immunology, 39–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60162-0_5.

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Schuler, Gerold, and Nikolaus Romani. "Generation of Mature Dendritic Cells from Human Blood." In Advances in Experimental Medicine and Biology, 7–13. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9966-8_2.

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Fanales-Belasio, Emanuele, Giovanna Zambruno, Andrea Cavani, and Giampiero Girolomoni. "Activation of Immature Dendritic Cells Via Membrane Sialophorin (CD43)." In Advances in Experimental Medicine and Biology, 207–12. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9966-8_35.

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Loh, Horace H., Andrew P. Smith, and Nancy M. Lee. "Effects of Opioids on Proliferation of Mature and Immature Immune Cells." In Advances in Experimental Medicine and Biology, 29–33. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2980-4_5.

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Häusser, G. A., C. Hultgren, K. Akagawa, Y. Tsunetsugu-Yokota, and A. Meyerhans. "Infection of Cultured Immature Dendritic Cells with Human Immunodeficiency Virus Type 1." In Advances in Experimental Medicine and Biology, 477–79. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1971-3_107.

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Ruedl, C., S. Hubele, C. Rieser, and H. Wolf. "The Role of CD11c+ Cells as Possible Candidates for Immature Dendritic Cells in the Murine Peyer’s Patches." In Advances in Experimental Medicine and Biology, 111–14. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9966-8_18.

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Yamashita, M., Y. Katakura, S. Matsumoto, T. Tamura, K. Teruya, and S. Shirahata. "Monocytes Suppress Immune Responses of Peripheral Blood Lymphocytes: Possible Implication of Immature Dendritic Cells." In Animal Cell Technology: Basic & Applied Aspects, 237–42. Dordrecht: Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-017-0726-8_41.

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Maraskovsky, Eugene, Bali Pulendran, Ken Brasel, Mark Teepe, Eileen R. Roux, Ken Shortman, Stewart D. Lyman, and Hilary J. Mckenna. "Dramatic Numerical Increase of Functionally Mature Dendritic Cells in FLT3 Ligand-Treated Mice." In Advances in Experimental Medicine and Biology, 33–40. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9966-8_6.

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Kaiserlian, D., K. Vidal, and J. P. Revillard. "Mature la+ murine intestinal epithelial cells with APC activity share common antigens with gut interdigitating dendritic cells." In Advances in Mucosal Immunology, 34–37. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1848-1_5.

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Zhou, Haixia, and Stanley Perlman. "Preferential Infection of Mature Dendritic Cells by the JHM Strain of Mouse Hepatitis Virus." In Advances in Experimental Medicine and Biology, 411–14. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/978-0-387-33012-9_74.

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Conference papers on the topic "Immature and mature dendritic cells"

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Jackson, C. W., N. K. Hutson, and S. A. Steward. "CHANGES IN PROTEIN SYNTHESIS PROFILES OF MEGAKARYOCYTES (MK) DURING MATURATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643545.

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Several key differentiation events occur within the recognizable MK compartment; however, little is known about the macromolecular changes responsible for these events. In this study, protein synthesis profiles of morphologically immature and mature guinea pig MK populations have been analyzed by twodimensional gel electrophoresis after in vivo labeling with 35S-methionine. MK were enriched by a bovine plasma aggregation enrichment procedure (Blood 69:173, 1987) and then fractionated into immature and mature populations based on differences in their respective buoyant densities (Brit. J. Haematol. 64:33, 1986). With this protocol, immature and mature MK populations were obtained in which MK constituted 95% of the cell mass. Ninety percent of the MK in the immature population had basophilic, immature morphology while ≥90% of those in the mature population had acidophilic, mature staining characteristics after Wright's staining. Protease inhibitors were used throughout the isolation procedure. The cells were solubilized and proteins subjected to two-dimensional electrophoresis according to O'Farrell (J. Biol. Chem. 250:4007, 1975). To examine basic proteins, proteins were electrophoresed in the first dimension under nonequilibrium conditions in a pH gradient as described by O'Farrell et al. (Cell 12:1133, 1977). Analyses of fluorograms revealed both qualitative and quantitative differences in synthesis profiles between these two MK populations. Among acidic proteins whose synthesis was readily detected in immature but not mature MK were ones whose MW and pi were respectively: 120K, 6.4; 7OK, 5.9; 70K, 6.9; 65K, 6.8; 55K, 6.2; 55K, 6.0; 53K, 5.8; 53K, 6.5; 52K, 6.7; 50K, 6.8; 41K, 5.5 and 33K, 6.7. Acidic and neutral proteins prominently synthesized in mature but not immature MK were found at MW and PI of: 110K, 5.7; 110K, 5.8 and 80K, 7.2. Basic proteins prominently synthesized in immature but not mature MK were found at MWs of: 110K; 70K; 52K; 48K; 39K and 18K. Basic proteins actively synthesized by mature but not immature MK had MWs of: 83K; 43K and 17K. These findings demonstrate that differences in protein synthesis patterns can be readily detected between immature and mature MK and provide baseline data with which to explore the role of these proteins in MK differentiation
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Cagnoni, Erika F., Ana Laura N. Carvalho, Marisa Dolhnikoff, Luiz F. F. Silva, Angela B. G. Santos, Maria C. R. Medeiros, Klaus Rabe, and Thais Mauad. "Mature CD83+ Dendritic Cells In Mediastinal Lymph Nodes Of Fatal Asthma." 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.a4401.

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Gannon, A. R., and D. J. Kelly. "The Changing Depth Dependant Properties of Articular Cartilage During Postnatal Development." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14514.

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During skeletal development and maturation compositional and architectural changes occur in articular cartilage. Specifically, the collagen architecture changes from a predominantly isotropic structure in immature articular cartilage to a mature arcade-like zonal structure first described by Benninghoff (1925)1,2,3. The goal of this study was to elucidate how the structure and composition of articular cartilage change during postnatal development and maturation and to relate this to the mechanical properties of the tissue, focusing in particular on how the key superficial region of the tissue adapts with age. To this end articular cartilage from a variety of age groups (one month old-immature, one year old-skeletally mature and three years old-fully mature) were subjected to increasing levels of strain. Local levels of deformation in the tissue were determined by fluorescently labelling and imaging cells that acted as fiducial markers. This enabled the local levels of strain and hence tissue mechanical properties to be determined with age and skeletal maturity.
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Fredriksson, K., X. Yao, JK Lam, HB Bhakta, and SJ Levine. "Exosomes Derived from Antigen-Pulsed Immature Dendritic Cells Attenuate Airway Inflammation and Hyperresponsiveness in a Murine Model of Allergic Asthma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3725.

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Nansai, Ryosuke, Mamoru Ogata, Junichi Takeda, Wataru Ando, Norimasa Nakamura, and Hiromichi Fujie. "Surface and Bulk Stiffness of the Mature Porcine Cartilage-Like Tissue Repaired With a Scaffold-Free, Stem Cell-Based Tissue Engineered Construct (TEC)." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204404.

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Since the healing capacity of articular cartilage is limited, it is important to develop cell-based therapies for the repair of cartilage. Although synthetic or animal-derived scaffolds are frequently used for effective cell delivery long-term safety and efficiency of such scaffolds still remain unclear. We have been developing a new tissue engineering technique for cartilage repair using a scaffold-free tissue engineered construct (TEC) bio-synthesized from synovium-derived mesenchymal stem cells (MSCs) [1]. As the TEC specimen is composed of cells with their native extracellular matrix, we believe that it is free from concern regarding long term immunological effects. Fujie et al. found in a micro indentation test using an atomic force microscope (AFM) that the immature porcine cartilage-like tissue repaired with TEC exhibited lower stiffness as compared with normal cartilage in immature porcine femur [2], although the macro-scale stiffness of the repaired tissue was almost same as that of the normal cartilage [3]. In the present study, we investigated the macro and micro-compressive properties of mature porcine cartilage-like tissue repaired with TEC.
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Truxova, Iva, Lenka Kasikova, Michal Hensler, Petr Skapa, Jan Laco, Ladislav Pecen, Lucie Belicova, et al. "Abstract A24: Mature dendritic cells correlate with favorable immune infiltrate and improved prognosis in ovarian carcinoma patients." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-a24.

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Truxova, Iva, Lenka Kasikova, Michal Hensler, Petr Skapa, Jan Laco, Ladislav Pecen, Lucie Belicova, et al. "Abstract B76: Mature dendritic cells correlate with favorable immune infiltrate and improved prognosis in ovarian carcinoma patients." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-b76.

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Susa, Tomoya, Ryosuke Nansai, Norimasa Nakamura, and Hiromichi Fujie. "Influence of Permeability on the Compressive Property of Articular Cartilage: A Scaffold-Free, Stem Cell-Based Therapy for Cartilage Repair." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53365.

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Since the healing capacity of articular cartilage is limited, it is important to develop cell-based therapies for the repair of cartilage. Although synthetic or animal-derived scaffolds are frequently used for effective cell delivery long-term safety and efficiency of such scaffolds still remain unclear. We have been studying on a scaffold-free tissue engineered construct (TEC) bio-synthesized from synovium-derived mesenchymal stem cells (MSCs) [1]. As the TEC specimen is composed of cells with their native extracellular matrix, we believe that it is free from concern regarding long term immunological effects. our previous studies indicated that a porcine partial thickness chondral defect was successfully repaired with TEC but that the compressive property of the TEC-treated cartilage-like repaired tissue was different from normal cartilage in both immature and mature animals. Imura et al. found that the permeability of the immature porcine cartilage-like tissues repaired with TEC recovered to normal level for 6 months except the superficial layer [2]. Therefore, the present study was performed to determine the depth-dependent permeability of mature porcine cartilage-like tissue repaired with TEC. Moreover, we investigated the effect of difference of permeability on the compressive property of articular cartilage using a finite element analysis (FEM).
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Nishimura, Junya, Hiroaki Tanaka, Yuichiro Miki, Tatsuro Tamura, Tatsunari Fukuoka, Go Ohira, Masatsune Shibutani, et al. "Abstract 2945: Impact of intratumoral mature dendritic cells on prognosis of the patients with esophageal squamous cell carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2945.

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Blank, Fabian, Peter Gerber, Alke Fink, Barbara Rothen-Rutishauser, Karin de Peyer, Thomas Geiser, Laurent Nicod, and Christophe von Garnier. "Dendritic Cells Exposed To Biomedical Nanoparticles Retain An Immature Like Functional State And Show Reduced Antigen Specific CD4+ T Cell Stimulation In Vitro." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3096.

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