Journal articles: '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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Hochreiter, Romana, Catherine Ptaschinski, Steven L. Kunkel, and Rosemary Rochford. "Murine gammaherpesvirus-68 productively infects immature dendritic cells and blocks maturation." Journal of General Virology 88, no. 7 (July 1, 2007): 1896–905. http://dx.doi.org/10.1099/vir.0.82931-0.

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Many viruses have evolved mechanisms to evade host immunity by subverting the function of dendritic cells (DCs). This study determined whether murine gammaherpesvirus-68 (γHV-68) could infect immature or mature bone-marrow-derived DCs and what effect infection had on DC maturation. It was found that γHV-68 productively infected immature DCs, as evidenced by increased viral titres over time. If DCs were induced to mature by exposure to LPS and then infected with γHV-68, only a small percentage of cells was productively infected. However, limiting-dilution assays to measure viral reactivation demonstrated that the mature DCs were latently infected with γHV-68. Electron microscopy revealed the presence of capsids in the nucleus of immature DCs but not in mature DCs. Interestingly, infection of immature DCs by γHV-68 did not result in upregulation of the co-stimulatory molecules CD80 and CD86 or MHC class I and II, or induce cell migration, suggesting that the virus infection did not induce DC maturation. Furthermore, γHV-68 infection of immature DCs did not result in elevated interleukin-12, an important cytokine in the induction of T-cell responses. Finally, lipopolysaccharide and poly(I : C) stimulation of γHV-68-infected immature DCs did not induce increases in the expression of co-stimulatory molecules and MHC class I or II compared with mock-treated cells, suggesting that γHV-68 infection blocked maturation. Taken together, these data demonstrate that γHV-68 infection of DCs differs depending on the maturation state of the DC. Moreover, the block in DC maturation suggests a possible immunoevasion strategy by γHV-68.

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Ferlazzo, Guido, Ming L. Tsang, Lorenzo Moretta, Giovanni Melioli, Ralph M. Steinman, and Christian Münz. "Human Dendritic Cells Activate Resting Natural Killer (NK) Cells and Are Recognized via the NKp30 Receptor by Activated NK Cells." Journal of Experimental Medicine 195, no. 3 (February 4, 2002): 343–51. http://dx.doi.org/10.1084/jem.20011149.

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During the innate response to many inflammatory and infectious stimuli, dendritic cells (DCs) undergo a differentiation process termed maturation. Mature DCs activate antigen-specific naive T cells. Here we show that both immature and mature DCs activate resting human natural killer (NK) cells. Within 1 wk the NK cells increase two– to fourfold in numbers, start secreting interferon (IFN)-γ, and acquire cytolytic activity against the classical NK target LCL721.221. The DC-activated NK cells then kill immature DCs efficiently, even though the latter express substantial levels of major histocompatibility complex (MHC) class I. Similar results are seen with interleukin (IL)-2–activated NK cell lines and clones, i.e., these NK cells kill and secrete IFN-γ in response to immature DCs. Mature DCs are protected from activated NK lysis, but lysis takes place if the NK inhibitory signal is blocked by a human histocompatibility leukocyte antigen (HLA)-A,B,C–specific antibody. The NK activating signal mainly involves the NKp30 natural cytotoxicity receptor, and not the NKp46 or NKp44 receptor. However, both immature and mature DCs seem to use a NKp30 independent mechanism to act as potent stimulators for resting NK cells. We suggest that DCs are able to control directly the expansion of NK cells and that the lysis of immature DCs can regulate the afferent limb of innate and adaptive immunity.

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Michiels, A., S. Tuyaerts, A. Bonehill, J. Corthals, K. Breckpot, C. Heirman, S. Van Meirvenne, et al. "Electroporation of immature and mature dendritic cells: implications for dendritic cell-based vaccines." Gene Therapy 12, no. 9 (March 3, 2005): 772–82. http://dx.doi.org/10.1038/sj.gt.3302471.

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Nagai, Taro. "Difference between Immature Dendritic Cells (imDCs) and Mature Dendritic Cells (mDCs) Derived from Human Monocytes." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 201.16. http://dx.doi.org/10.4049/jimmunol.198.supp.201.16.

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Abstract We induced imDCs and mDCs from human monocytes. Then we examined their surface markers and cytokine secretion to compare with their functions. Surface Markers Monocytes marker CD14 still expressed on imDCs and disappeared on mDCs. However, DC marker CD209 expressed on both imDCs and mDCs as same amount. Co-stimulatory molecules, such as CD40, CD80, CD86, and HLA Class II, expressed on mDCs more than imDCs. So, we expected that imDCs cannot induce T cell proliferation and differentiation because Cytokine Secretion We stimulated imDCs and mDCs by CD40L transfected L cells with or without several kinds of cytokine for 2days and measured cytokine secretion from them by ELISA. mDCs secreted more IL-27 than imDCs, however IL-6, IL-12p70, and IL-23 secretion from them were almost same. Effects of adding cytokines on stimulation were almost same as on imDCs and mDCs. IFN-γ enhanced IL-12p70 secretion, however almost no effects against IL-6, IL-23, and IL-27 secretion. IL-4 and IL-13, which induce Th2 differentiation, had almost no effect against IL-6 and IL-27 secretion and suppressed secretions of IL-23 which induce Th17 differentiation, however enhanced secretion of IL-12 p70 which induce Th1 differentiation. These results suggest that even though imDC may be able to induce T cell proliferation and differentiation because they secrete enough amount of cytokines for it. Next, we would like to co-culture DCs and naive Th cells to confirm whether imDCs can induce T cell proliferation and differentiation or not.

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Jonuleit, Helmut, Edgar Schmitt, Gerold Schuler, Jürgen Knop, and Alexander H. Enk. "Induction of Interleukin 10–Producing, Nonproliferating Cd4+ T Cells with Regulatory Properties by Repetitive Stimulation with Allogeneic Immature Human Dendritic Cells." Journal of Experimental Medicine 192, no. 9 (October 30, 2000): 1213–22. http://dx.doi.org/10.1084/jem.192.9.1213.

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The functional properties of dendritic cells (DCs) are strictly dependent on their maturational state. To analyze the influence of the maturational state of DCs on priming and differentiation of T cells, immature CD83− and mature CD83+ human DCs were used for stimulation of naive, allogeneic CD4+ T cells. Repetitive stimulation with mature DCs resulted in a strong expansion of alloreactive T cells and the exclusive development of T helper type 1 (Th1) cells. In contrast, after repetitive stimulation with immature DCs the alloreactive T cells showed an irreversibly inhibited proliferation that could not be restored by restimulation with mature DCs or peripheral blood mononuclear cells, or by the addition of interleukin (IL)-2. Only stimulation of T cells with mature DCs resulted in an upregulation of CD154, CD69, and CD70, whereas T cells activated with immature DCs showed an early upregulation of the negative regulator cytotoxic T lymphocyte–associated molecule 4 (CTLA-4). These T cells lost their ability to produce interferon γ, IL-2, or IL-4 after several stimulations with immature DCs and differentiated into nonproliferating, IL-10–producing T cells. Furthermore, in coculture experiments these T cells inhibited the antigen-driven proliferation of Th1 cells in a contact- and dose-dependent, but antigen-nonspecific manner. These data show that immature and mature DCs induce different types of T cell responses: inflammatory Th1 cells are induced by mature DCs, and IL-10–producing T cell regulatory 1–like cells by immature DCs.

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Leslie, David S., Michael S. Vincent, Franca M. Spada, Hiranmoy Das, Masahiko Sugita, Craig T. Morita, and Michael B. Brenner. "CD1-mediated γ/δ T Cell Maturation of Dendritic Cells." Journal of Experimental Medicine 196, no. 12 (December 9, 2002): 1575–84. http://dx.doi.org/10.1084/jem.20021515.

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Immature myeloid dendritic cells (DCs) express only low levels of major histocompatibility complex (MHC) class II but express high levels of CD1 a, b, and c antigen-presenting molecules at the cell surface. As Vδ1+ γ/δ T cells are the main tissue subset of γ/δ T cells and they are known to recognize CD1c in the absence of specific foreign antigen recognition, we examined the possible interaction of these T cells with immature DCs. We show that CD1-restricted γ/δ T cells can mediate the maturation of DCs. DC maturation required cell–cell contact and could be blocked by antibodies against CD1c. The maturation process was partially mediated by tumor necrosis factor α. Importantly, immature DCs matured in the presence of lipopolysaccharide and CD1-restricted γ/δ T cells produced bioactive interleukin-12p70. In addition, these DCs were able to efficiently present peptide antigens to naive CD4+ T cells. CD1-restricted γ/δ T cell recognition of immature DCs provides the human immune system with the capacity to rapidly generate a pool of mature DCs early during microbial invasion. This may be an important source of critical host signals for T helper type 1 polarization of antigen-specific naive T cells and the subsequent adaptive immune response.

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Rosolem, Mayara C., Rosemeri O. Vasconcelos, Eduardo Garrido, Thaís L. L. Castanheira, Pamela R. R. Moreira, Geórgia M. Magalhães, Daniela B. Rozza, and Salvador B. Ramos. "Immunodetection of myeloid and plasmacytoid dendritic cells in mammary carcinomas of female dogs." Pesquisa Veterinária Brasileira 35, no. 11 (November 2015): 906–12. http://dx.doi.org/10.1590/s0100-736x2015001100006.

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ABSTRACT: Dendritic cells have attracted great interest from researchers as they may be used as targets of tumor immune evasion mechanisms. The main objective of this study was to evaluate the relationship between the dendritic cells (DCs) subpopulation in simple type mammary carcinomas in female dogs. Two groups of samples were used: the control group consisted of 18 samples of mammary tissue without changes and the tumor group with 26 simple type mammary carcinomas. In these groups, we evaluated the immunodetection of immature and mature myeloid DCs, plasmacytoid DCs and MHC-II. In mammary tumor, mature myeloid DCs predominated in the peritumoral region, while immature myeloid DCs and plasmacytoid DCs were evident in the intratumoral region. Immunostaining of MHC-II was visualized in mammary acini (control group), in tumor cells and inflammatory infiltration associated with tumors. The comparison between the control and tumor groups showed a statistically significant difference between immature myeloid DCs, mature myeloid DCs and plasmacytoid DCs. The immunodetection of MHC-II was not significant when comparing the groups. The predominance of immature DCs in the tumor group is possibly related to an inefficient immune response, promoting the development and survival of tumor cells. The presence of plasmacytoid DCs in the same group suggests a worse prognosis for female dogs with mammary tumors. Therefore, the ability of differentiation of canine dendritic cells could be influenced by neoplastic cells and by the tumor microenvironment.

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Lissoni, P., F. Brivio, R. Ferrante, L. Vigore, M. Vaghi, E. Fumagalli, R. Bucovec, F. Malugani, and L. Fumagalli. "Circulating Immature and Mature Dendritic Cells in Relation to Lymphocyte Subsets in Patients with Gastrointestinal Tract Cancer." International Journal of Biological Markers 15, no. 1 (January 2000): 22–25. http://dx.doi.org/10.1177/172460080001500104.

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Cancer-related deficiency in circulating dendritic cells (DC), whose important anticancer role is well established, has been proven to be associated with lymphocytopenia. This study was performed to evaluate which lymphocyte subset is most markedly related to the failure of the DC system. The study included 30 patients with gastrointestinal tract cancer, 10 of whom had distant organ metastases. Immature and mature DCs were measured by FACS and monoclonal antibodies against CD123 and CD11c antigens, respectively. Low levels of immature and mature DCs were observed in 63% and 43% of patients, respectively. Patients with low levels of circulating mature DCs had significantly lower values of T lymphocytes, T helper lymphocytes and NK cells than those with normal mature DC levels. In contrast, no significant difference was seen between patients with normal or abnormally low values of immature DCs. Conversely, patients with a decreased number of T lymphocytes, T helper lymphocytes and NK cells showed significantly lower values of circulating mature DCs than those with lymphocyte subsets within the normal range, whereas no difference was seen in immature DC amounts. This study suggests that only mature DC deficiency may be associated with important lymphocyte subset alterations in cancer patients, whereas deficiency in immature DCs does not seem to be related to other immune cell disorders.

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Wilson, Nicholas S., Dima El-Sukkari, Gabrielle T. Belz, Christopher M. Smith, Raymond J. Steptoe, William R. Heath, Ken Shortman, and José A. Villadangos. "Most lymphoid organ dendritic cell types are phenotypically and functionally immature." Blood 102, no. 6 (September 15, 2003): 2187–94. http://dx.doi.org/10.1182/blood-2003-02-0513.

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Abstract Dendritic cells (DCs) have been thought to follow a life history, typified by Langerhans cells (LCs), with 2 major developmental stages: an immature stage that captures antigens in the periphery and a mature stage that presents those antigens in the lymphoid organs. However, a systematic assessment of the maturity of lymphoid organ DCs has been lacking. We have analyzed the maturity of the DC types found in the steady state in the spleen, lymph nodes (LNs), and thymus. The DCs that migrate into the iliac, mesenteric, mediastinal, or subcutaneous LNs from peripheral tissues were mature and therefore could not process and present newly encountered antigens. However, all the other DC types were phenotypically and functionally immature: they expressed low levels of surface major histocompatibility complex class II (MHC II) and CD86, accumulated MHC II in their endosomes, and could present newly encountered antigens. These immature DCs could be induced to mature by culture in vitro or by inoculation of inflammatory stimuli in vivo. Therefore, the lymphoid organs contain a large cohort of immature DCs, most likely for the maintenance of peripheral tolerance, which can respond to infections reaching those organs and mature in situ.

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Kim, Min Kyung, and Jaeyun Kim. "Properties of immature and mature dendritic cells: phenotype, morphology, phagocytosis, and migration." RSC Advances 9, no. 20 (2019): 11230–38. http://dx.doi.org/10.1039/c9ra00818g.

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Segura, Elodie, Carole Nicco, Bérangère Lombard, Philippe Véron, Graça Raposo, Frédéric Batteux, Sebastian Amigorena, and Clotilde Théry. "ICAM-1 on exosomes from mature dendritic cells is critical for efficient naive T-cell priming." Blood 106, no. 1 (July 1, 2005): 216–23. http://dx.doi.org/10.1182/blood-2005-01-0220.

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Exosomes are secreted vesicles formed in late endocytic compartments. Immature dendritic cells (DCs) secrete exosomes, which transfer functional major histocompatibility complex (MHC)–peptide complexes to other DCs. Since immature and mature DCs induce different functional T-cell responses (ie, tolerance versus priming), we asked whether DC maturation also influenced the priming abilities of their exosomes. We show that exosomes secreted by lipopolysaccharide (LPS)–treated mature DCs are 50- to 100-fold more potent to induce antigen-specific T-cell activation in vitro than exosomes from immature DCs. In vitro, exosomes from mature DCs transfer to B lymphocytes the ability to prime naive T cells. In vivo, only mature exosomes trigger effector T-cell responses, leading to fast skin graft rejection. Proteomic and biochemical analyses revealed that mature exosomes are enriched in MHC class II, B7.2, intercellular adhesion molecule 1 (ICAM-1), and bear little milk-fat globule–epidermal growth factor–factor VIII (MFG-E8) as compared with immature exosomes. Functional analysis using DC-derived exosomes from knock-out mice showed that MHC class II and ICAM-1 are required for mature exosomes to prime naive T cells, whereas B7.2 and MFG-E8 are dispensable. Therefore, changes in protein composition and priming abilities of exosomes reflect the maturation signals received by DCs.

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Lutz, Manfred B., and Gerold Schuler. "Immature, semi-mature and fully mature dendritic cells: which signals induce tolerance or immunity?" Trends in Immunology 23, no. 9 (September 2002): 445–49. http://dx.doi.org/10.1016/s1471-4906(02)02281-0.

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Ridolfi, R., A. Riccobon, M. Petrini, L. Ridolfi, L. Fiammenghi, M. Stefanelli, M. Selva, and D. Amadori. "Comparison between immature and mature dendritic cells in a vaccination trial." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 2562. http://dx.doi.org/10.1200/jco.2004.22.14_suppl.2562.

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Ridolfi, R., A. Riccobon, M. Petrini, L. Ridolfi, L. Fiammenghi, M. Stefanelli, M. Selva, and D. Amadori. "Comparison between immature and mature dendritic cells in a vaccination trial." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 2562. http://dx.doi.org/10.1200/jco.2004.22.90140.2562.

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Souto, Elizabeth Xisto. "Determination of Reference Values of Hematopoetic CELLS in Normal BONE Marrow By 10 Colors FLOW Cytometry in Brazilian Population." Blood 142, Supplement 1 (November 28, 2023): 5592. http://dx.doi.org/10.1182/blood-2023-179486.

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Purpose: To determine relative and absolute reference values of normality in individuals with no hematologic disease bone marrow, as well as normal patterns of maturation for the different hematopoietic lineages. Methods: Bone marrow samples were collected from 46 healthy patients (16 women and 30 men) undergoing orthopedic surgery and were aged between 18 and 87 years (median 36 years). The analysis of 8 tubes performed in an equipment with 10 colors configuration enabled to evaluate and quantify (% and mm³) B lymphocytes (immature and mature), T lymphocytes (helper, cytotoxic, double negative, double positive), natural killer cells, granulocytes (myeloblasts, promyelocytes, myelocytes, metamyelocytes, rods and neutrophils), monocytes (monoblasts, promonocytes, mature monocytes, classical, intermediate and non-classical), erythroblasts (immature and mature), plasma cells, basophils, mast cells, myeloid dendritic cells and plasmacytoid dendritic cells. The results were evaluated according to sex (female and male), age group (<40, 40 to 60, >60 years), and described as median percentage and absolute values. Results: In evaluating the results according to age group, we identified that older individuals presented an increase in plasma cells that expressed CD56 (p=0.031 in absolute values). In addition, they also had increase relation of CD4/CD8 ratio (p=0.002), mast cells (p=0.004 in percentages), non-classical monocytes (p=0.016 in percentages), as well as a decrease in cytotoxic T lymphocytes (p=0.031 in absolute values), double negative T lymphocytes (p=0.018 in absolute values), and natural killer cells that express CD56 (p =0.002 in absolute values and p=0.012 in percentages). Moreover, these individuals also presented higher natural killer cells that expressed CD56 and CD16 (p=0.024 in absolute values), myeloblasts (p=0.048 in absolute values), metamyelocytes/Rods (p=0.038 in absolute values), neutrophils (p=0.006 in absolute values), monoblasts (p=0.030 in absolute values), mature monocytes (p=0.024 in absolute values), classical monocytes (p=0.017), plasmacytoid dendritic cells (p=0.027 in absolute values), and mature erythroblasts (p=0.004 in absolute values). In the evaluation of the results according to sex, we identified that the population of mature B lymphocytes (p=0.013) and B lymphocytes that expressed CD5 (p=0.014) was higher in women, while the percentage of natural killer cells was relatively higher than in men (p=0.007), particularly in the population of cells that expressed CD56 and CD16 (p=0.013). Conclusion: This study established reference values (absolute and relative) of B lymphocytes (immature and mature), T lymphocytes (helper, cytotoxic, double negative, double positive), natural killer cells, granulocytes (myeloblasts, promyelocytes, myelocytes, metamyelocytes, rods and neutrophils), monocytes (monoblasts, promonocytes, mature monocytes, classical, intermediate and non-classical), erythroblasts (immature and mature), plasma cells, basophils, mast cells, myeloid dendritic cells and plasmacytoid dendritic cells according sex and age group in bone marrow samples from individuals with no hematologic disease Maturational stages of B lymphocytes, granulocytes, monocytes and erythroblasts was shown to be stable regardless of sex and age.

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Nobile, Cinzia, Marianne Lind, Francesc Miro, Karine Chemin, Marie Tourret, Giovanni Occhipinti, Stéphanie Dogniaux, Sebastian Amigorena, and Claire Hivroz. "Cognate CD4+ T-cell–dendritic cell interactions induce migration of immature dendritic cells through dissolution of their podosomes." Blood 111, no. 7 (April 1, 2008): 3579–90. http://dx.doi.org/10.1182/blood-2007-08-107755.

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Abstract Dendritic cells (DCs) control T cell–based immunity. To do so they need to mature and migrate to sites of T-cell priming. We have previously shown that cognate interactions of human CD4+ T cells with DCs induce DC maturation. We show here that CC chemokines produced during antigen-specific T-DC interactions also induce strong morphologic modifications and migration of immature DCs. These modifications are required for efficient T-cell activation. Moreover, we show that CC chemokines produced during antigen-specific DC–T-cell interactions induce the dissolution of structures involved in cell motility and present on immature DCs (ie, podosomes). We thus propose a model in which chemokines secreted during Ag-specific contact between T cells and DCs induce disassembly of interacting and neighboring immature DC podosomes, leading to recruitment of more immature DCs toward sites of antigenic stimulation and to amplification of T-cell responses.

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McKimmie, Clive S., Mark D. Singh, Kay Hewit, Oscar Lopez-Franco, Michelle Le Brocq, Stefan Rose-John, Kit Ming Lee, et al. "An analysis of the function and expression of D6 on lymphatic endothelial cells." Blood 121, no. 18 (May 2, 2013): 3768–77. http://dx.doi.org/10.1182/blood-2012-04-425314.

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Key Points D6 regulates the ability of lymphatic endothelial cells to discriminate between mature and immature dendritic cells. D6 expression is regulated by inflammatory cytokines indicative of a preferential role in inflamed conditions.

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de Goër de Herve, Marie-Ghislaine, Deniz Durali, Tú-Anh Tran, Gwénola Maigné, Federico Simonetta, Philippe Leclerc, Jean-François Delfraissy, and Yassine Taoufik. "Differential effect of agonistic anti-CD40 on human mature and immature dendritic cells: the Janus face of anti-CD40." Blood 106, no. 8 (October 15, 2005): 2806–14. http://dx.doi.org/10.1182/blood-2004-12-4678.

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AbstractAgonistic monoclonal antibodies to CD40 (CD40 mAbs) have a puzzling dual therapeutic effect in experimental animal models. CD40 mAbs induce tumor regression by potentiating antitumoral T-cell responses, yet they also have immunosuppressive activity in chronic autoimmune inflammatory processes. CD40 mAbs are thought to act on antigen presentation by dendritic cells (DCs) to T cells. DCs can be distinguished as either immature or mature by their phenotype and their ability to generate an effective T-cell response. Here we found that, on human cells, although anti-CD40 led immature DCs to mature and became immunogenic, it also reduced the capacity of lipopolysaccharide (LPS) and tumor necrosis factor α (TNF-α)-matured DCs to generate a specific CD4 T-cell response. This inhibitory effect was related to rapid and selective apoptosis of mature DCs. Anti-CD40-mediated apoptosis was due to an indirect mechanism involving cooperation with the death domain-associated receptor Fas, leading to activation of Fas-associated death domain protein (FADD) and caspase-8. On human cells, CD40 activation by such agonists could, therefore, trigger immune responses to antigens presented by immature DCs, which are otherwise nonimmunogenic, by inducing maturation. On the other hand, anti-CD40 mAbs, by rapidly inducing apoptosis, may reduce the capacity of inflammatory signal-matured immunogenic DCs to generate an effective T-cell response. These results call for caution in CD40 mAb-based immunotherapy strategies. (Blood. 2005;106:2806-2814)

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Riedl, Elisabeth, Johannes Stöckl, Otto Majdic, Clemens Scheinecker, Walter Knapp, and Herbert Strobl. "Ligation of E-cadherin on in vitro–generated immature Langerhans-type dendritic cells inhibits their maturation." Blood 96, no. 13 (December 15, 2000): 4276–84. http://dx.doi.org/10.1182/blood.v96.13.4276.

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Abstract Epithelial tissues of various organs contain immature Langerhans cell (LC)-type dendritic cells, which play key roles in immunity. LCs reside for long time periods at an immature stage in epithelia before migrating to T-cell–rich areas of regional lymph nodes to become mature interdigitating dendritic cells (DCs). LCs express the epithelial adhesion molecule E-cadherin and undergo homophilic E-cadherin adhesion with surrounding epithelial cells. Using a defined serum-free differentiation model of human CD34+hematopoietic progenitor cells, it was demonstrated that LCs generated in vitro in the presence of transforming growth factor β1 (TGF-β1) express high levels of E-cadherin and form large homotypic cell clusters. Homotypic LC clustering can be inhibited by the addition of anti–E- cadherin monoclonal antibodies (mAbs). Loss of E-cadherin adhesion of LCs by mechanical cluster disaggregation correlates with the rapid up-regulation of CD86, neo-expression of CD83, and diminished CD1a cell surface expression by LCs—specific phenotypic features of mature DCs. Antibody ligation of E-cadherin on the surfaces of immature LCs after mechanical cluster disruption strongly reduces the percentages of mature DCs. The addition of mAbs to the adhesion molecules LFA-1 or CD31 to parallel cultures similarly inhibits homotypic LC cluster formation, but, in contrast to anti–E-cadherin, these mAbs fail to inhibit DC maturation. Thus, E-cadherin engagement on immature LCs specifically inhibits the acquisition of mature DC features. E-cadherin–mediated LC maturation suppression may represent a constitutive active epithelial mechanism that prevents the uncontrolled maturation of immature LCs.

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30

Riedl, Elisabeth, Johannes Stöckl, Otto Majdic, Clemens Scheinecker, Walter Knapp, and Herbert Strobl. "Ligation of E-cadherin on in vitro–generated immature Langerhans-type dendritic cells inhibits their maturation." Blood 96, no. 13 (December 15, 2000): 4276–84. http://dx.doi.org/10.1182/blood.v96.13.4276.h8004276_4276_4284.

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Epithelial tissues of various organs contain immature Langerhans cell (LC)-type dendritic cells, which play key roles in immunity. LCs reside for long time periods at an immature stage in epithelia before migrating to T-cell–rich areas of regional lymph nodes to become mature interdigitating dendritic cells (DCs). LCs express the epithelial adhesion molecule E-cadherin and undergo homophilic E-cadherin adhesion with surrounding epithelial cells. Using a defined serum-free differentiation model of human CD34+hematopoietic progenitor cells, it was demonstrated that LCs generated in vitro in the presence of transforming growth factor β1 (TGF-β1) express high levels of E-cadherin and form large homotypic cell clusters. Homotypic LC clustering can be inhibited by the addition of anti–E- cadherin monoclonal antibodies (mAbs). Loss of E-cadherin adhesion of LCs by mechanical cluster disaggregation correlates with the rapid up-regulation of CD86, neo-expression of CD83, and diminished CD1a cell surface expression by LCs—specific phenotypic features of mature DCs. Antibody ligation of E-cadherin on the surfaces of immature LCs after mechanical cluster disruption strongly reduces the percentages of mature DCs. The addition of mAbs to the adhesion molecules LFA-1 or CD31 to parallel cultures similarly inhibits homotypic LC cluster formation, but, in contrast to anti–E-cadherin, these mAbs fail to inhibit DC maturation. Thus, E-cadherin engagement on immature LCs specifically inhibits the acquisition of mature DC features. E-cadherin–mediated LC maturation suppression may represent a constitutive active epithelial mechanism that prevents the uncontrolled maturation of immature LCs.

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Pion, Marjorie, Romaine Stalder, Rafael Correa, Bastien Mangeat, Greg J. Towers, and Vincent Piguet. "Identification of an Arsenic-Sensitive Block to Primate Lentiviral Infection of Human Dendritic Cells." Journal of Virology 81, no. 21 (August 29, 2007): 12086–90. http://dx.doi.org/10.1128/jvi.00800-07.

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ABSTRACT Dendritic cells are central to the early events of human immunodeficiency virus type 1 (HIV-1) transmission, but HIV-1 infects dendritic cells inefficiently in vitro compared to activated CD4+ T cells. There is a strong postentry restriction of HIV-1 infection in dendritic cells, partly mediated by the cellular restriction factor APOBEC3G. Here, we reveal that arsenic trioxide markedly increases HIV infection of immature and mature dendritic cells as well as blood-derived myeloid dendritic cells in an APOBEC3G- and TRIM5α-independent way. Our data suggest the presence of powerful, arsenic-sensitive antiviral activities in primary human immune cells of the dendritic cell lineage.

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32

Körner, Ulrich, Veronika Fuss, Jutta Steigerwald, and Heidrun Moll. "Biogenesis of Leishmania major-Harboring Vacuoles in Murine Dendritic Cells." Infection and Immunity 74, no. 2 (February 2006): 1305–12. http://dx.doi.org/10.1128/iai.74.2.1305-1312.2006.

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ABSTRACT In mammalian hosts, Leishmania sp. parasites are obligatory intracellular organisms that invade macrophages and dendritic cells (DC), where they reside in endocytic organelles termed parasitophorous vacuoles (PV). Most of the present knowledge of the characteristics of PV harboring Leishmania sp. is derived from studies with infected macrophages. Since DC play a key role in host resistance to leishmaniasis, there is a need to understand the properties and biogenesis of PV in Leishmania sp.-infected DC. Therefore, we determined the acquisition of endosomal and lysosomal molecules by Leishmania major-containing compartments in DC at different maturation stages, using fluorescence labeling and confocal microscopy. The results show that newly formed phagosomes in DC rapidly develop into late endosomal compartments. However, the small GTPase Rab7, which regulates late fusion processes, was found only in PV of mature bone marrow-derived DC (BMDC); it was absent in immature BMDC, suggesting an arrest of their PV biogenesis at the stage of late endosomes. Indeed, fusion assays with endocytic tracers demonstrated that the fusion activity of L. major-harboring PV toward lysosomes is higher in mature BMDC than in immature BMDC. The inhibition of PV-lysosome fusion in DC is dependent upon the viability and life cycle stage of the parasite, because live promastigotes blocked the fusion almost completely, whereas killed organisms and amastigotes induced a considerable level of fusion activity. The differences in the fusion competences of immature and mature DC may be relevant for their distinct functional activities in the uptake, transport, and presentation of parasite antigens.

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Mittelbrunn, María, Gloria Martínez del Hoyo, María López-Bravo, Noa B. Martín-Cofreces, Alix Scholer, Stéphanie Hugues, Luc Fetler, Sebastián Amigorena, Carlos Ardavín, and Francisco Sánchez-Madrid. "Imaging of plasmacytoid dendritic cell interactions with T cells." Blood 113, no. 1 (January 1, 2009): 75–84. http://dx.doi.org/10.1182/blood-2008-02-139865.

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Abstract Plasmacytoid dendritic cells (pDCs) efficiently produce type I interferon and participate in adaptive immune responses, although the molecular interactions between pDCs and antigen-specific T cells remain unknown. This study examines immune synapse (IS) formation between murine pDCs and CD4+ T cells. Mature pDCs formed canonical ISs, involving relocation to the contact site of the microtubule-organizing center, F-actin, protein kinase C-θ, and pVav, and activation of early signaling molecules in T cells. However, immature pDCs were less efficient at forming conjugates with T cells and inducing IS formation, microtubule-organizing center translocation, and T-cell signaling and activation. Time-lapse videomicroscopy and 2-photon in vivo imaging of pDC–T-cell interactions revealed that immature pDCs preferentially mediated transient interactions, whereas mature pDCs promoted more stable contacts. Our data indicate that, under steady-state conditions, pDCs preferentially establish transient contacts with naive T cells and show a very modest immunogenic capability, whereas on maturation, pDCs are able to form long-lived contacts with T cells and significantly enhance their capacity to activate these lymphocytes.

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Kaneider, Nicole C., Arthur Kaser, Stefan Dunzendorfer, Herbert Tilg, and Christian J. Wiedermann. "Sphingosine Kinase-Dependent Migration of Immature Dendritic Cells in Response to Neurotoxic Prion Protein Fragment." Journal of Virology 77, no. 9 (May 1, 2003): 5535–39. http://dx.doi.org/10.1128/jvi.77.9.5535-5539.2003.

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ABSTRACT The concept that circulating dendritic cells mediate neuroinvasion in transmissible spongiform encephalopathies received strong support from recent observations that prion protein is expressed in myeloid dendritic cells. We observed that prion protein fragment 106-126 is a chemoattractant for monocyte-derived immature but not mature dendritic cells. Signaling events in chemotaxis involved enzymes downstream of Gq protein and were inhibited by blockade of sphingosine kinase, suggesting transactivation of sphingosine-1-phosphate-dependent cell motility by prion protein.

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35

Cremer, Isabelle, Marie-Caroline Dieu-Nosjean, Sylvie Maréchal, Colette Dezutter-Dambuyant, Sarah Goddard, David Adams, Nathalie Winter, et al. "Long-lived immature dendritic cells mediated by TRANCE-RANK interaction." Blood 100, no. 10 (November 15, 2002): 3646–55. http://dx.doi.org/10.1182/blood-2002-01-0312.

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Immature dendritic cells (DCs) reside in interstitial tissues (int-DC) or in the epidermis, where they capture antigen and, thereafter, mature and migrate to draining lymph nodes (LNs), where they present processed antigen to T cells. We have identified int-DCs that express both TRANCE (tumor necrosis factor–related activation-induced cytokine) and RANK (receptor activator of NF-κB) and have generated these cells from CD34+ human progenitor cells using macrophage colony-stimulating factor (M-CSF). These CD34+-derived int-DCs, which are related to macrophages, are long-lived, but addition of soluble RANK leads to significant reduction of cell viability and Bcl-2 expression. This suggests that constitutive TRANCE-RANK interaction is responsible for CD34+-derived int-DC longevity. Conversely, CD1a+ DCs express only RANK and are short-lived. However, they can be rescued from cell death either by recombinant soluble TRANCE or by CD34+-derived int-DCs. CD34+-derived int-DCs mature in response to lipopolysaccharide (LPS) plus CD40 ligand (L) and become capable of CCL21/CCL19-mediated chemotaxis and naive T-cell activation. Upon maturation, they lose TRANCE, making them, like CD1a+DCs, dependent on exogenous TRANCE for survival. These findings provide evidence that TRANCE and RANK play important roles in the homeostasis of DCs.

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Zhou, Haixia, and Stanley Perlman. "Preferential Infection of Mature Dendritic Cells by Mouse Hepatitis Virus Strain JHM." Journal of Virology 80, no. 5 (March 1, 2006): 2506–14. http://dx.doi.org/10.1128/jvi.80.5.2506-2514.2006.

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ABSTRACT Mouse hepatitis virus strain JHM (MHV-JHM) causes acute encephalitis and acute and chronic demyelinating diseases in mice. Dendritic cells (DCs) are key cells in the initiation of innate and adaptive immune responses, and infection of these cells could potentially contribute to a dysregulated immune response; consistent with this, recent results suggest that DCs are readily infected by another strain of mouse hepatitis virus, the A59 strain (MHV-A59). Herein, we show that the JHM strain also productively infected DCs. Moreover, mature DCs were at least 10 times more susceptible than immature DCs to infection with MHV-JHM. DC function was impaired after MHV-JHM infection, resulting in decreased stimulation of CD8 T cells in vitro. Preferential infection of mature DCs was not due to differential expression of the MHV-JHM receptor CEACAM-1a on mature or immature cells or to differences in apoptosis. Although we could not detect infected DCs in vivo, both CD8+ and CD11b+ splenic DCs were susceptible to infection with MHV-JHM directly ex vivo. This preferential infection of mature DCs may inhibit the development of an efficient immune response to the virus.

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Granelli-Piperno, Angela, Elena Delgado, Victoria Finkel, William Paxton, and Ralph M. Steinman. "Immature Dendritic Cells Selectively Replicate Macrophagetropic (M-Tropic) Human Immunodeficiency Virus Type 1, while Mature Cells Efficiently Transmit both M- and T-Tropic Virus to T Cells." Journal of Virology 72, no. 4 (April 1, 1998): 2733–37. http://dx.doi.org/10.1128/jvi.72.4.2733-2737.1998.

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ABSTRACT Dendritic cells (DCs) can develop from CD14+ peripheral blood monocytes cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4). By 6 days in culture, the cells have the characteristics of immature DCs and can be further induced to mature by inflammatory stimuli or by monocyte-conditioned medium. After infection with macrophagetropic (M-tropic) human immunodeficiency virus type 1 (HIV-1), monocytes and mature DCs show a block in reverse transcription and only form early transcripts that can be amplified with primers for the R/U5 region. In contrast, immature DCs cultured for 6 or 11 days in GM-CSF and IL-4 complete reverse transcription and show a strong signal when LTR/gag primers are used. Blood monocytes and mature DCs do not replicate HIV-1, whereas immature DCs can be productively infected, but only with M-tropic HIV-1. The virus produced by immature DCs readily infects activated T cells. Although mature DCs do not produce virus, these cells transmit both M- and T-tropic virus to T cells. In the cocultures, both DCs and T cells must express functional chemokine coreceptors for viral replication to occur. Therefore, the developmental stage of DCs can influence the interaction of these cells with HIV-1 and influence the extent to which M-tropic and T-tropic virus can replicate.

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Avigan, David, Baldev Vasir, Zekui Wu, Lynne Uhl, Therese Desliva, Jacalyn Rosenblatt, James D. Levine, et al. "Dendritic Cell Myeloma Fusions Stimulate Anti-Tumor Immunity: Results from Pre-Clinical Studies and a Clinical Trial." Blood 104, no. 11 (November 16, 2004): 751. http://dx.doi.org/10.1182/blood.v104.11.751.751.

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Abstract Dendritic cell (DC)-tumor fusions effectively present a broad array of tumor associated antigens in the context of DC derived costimulation. Vaccination with fusion cells induces tumor specific immunity in animal models and clinical studies. We have examined the antigen presenting characteristics of DCs fused with myeloma cells. Immature DCs were generated by culturing adherent mononuclear cells with GM-CSF and IL-4 for 1 week. Maturation was induced by exposure to TNFa for 48 hours. Compared to immature DCs, patient derived mature DC had decreased CD14 expression, increased expression of CD80 and CD83 and increased mean flourescent intensity of CD86. Using polyethyelene glycol (PEG), monocyte derived immature and mature DCs were fused to myeloma cells derived from human cell lines and patient derived bone marrow specimens. Fusion cells were isolated by flow cytometric gating of cells that co-expressed unique DC and tumor antigens. For both immature and mature DC populations, cell fusion was associated with marked upregulation of costimulatory and maturation markers. Mean expression of CD86 was 98% in both fusion cell populations and CD83 was observed in 86% and 84% of immature and mature DC/myeloma fusions, respectively. Immature and mature DC/myeloma fusions prominently express IL-12 (mean 48% and 50%, respectively) and the chemokine receptor, CCR7 (mean 33% and 46%, respectively), necessary for the migration to sites of T cell traffic in the draining lymph node. DC/myeloma fusions induce IFNγ expression by autologous T cells. In 5 serial studies, immature and mature DC/myeloma fusion cells prominently stimulate cytotoxic T lymphocyte mediated lysis of tumor targets (mean 45% and 57%, respectively). Based on these findings we have initiated a clinical trial in which successive cohorts of patients with multiple myeloma undergo vaccination with myeloma cells fused with autologous mature DCs administered in conjunction with GM-CSF. Patients with clinically stable disease who demonstrate at least 20% marrow involvement with plasma cells are potentially eligible. DCs are generated from adherent mononuclear cells collected by leukapheresis that are cultured with GM-CSF, IL-4 and TNFa. Myeloma cells are obtained from short-term culture of bone marrow aspirate specimens. DCs and myeloma cells are co-cultured in the presence of PEG and fusion cells are quantified by identifying cells that co-express DC (CD86, CD83) and myeloma (CD38, CD138) antigens. To date, 6 patients have been enrolled of which 4 have been vaccinated; 3 with 1x10(6) and 1 with 2 x 10(6) fusion cells. Mean yields of DC, tumor, and fusion cells were 7.64 x107, 1.87 x107, and 6.12 x106 cells, respectively. In contrast to myeloma cells, DC and fusion cells preparations prominently induced allogeneic T cell proliferation with mean stimulation indices of 47 and 50, respectively. Toxicities judged to be potentially vaccine related have been mild and include muscle aches/stiffness, transient fever, pruritis, rash and fatigue. Vaccination resulted in the induction of tumor specific immunity as determined by increased percentage of CD4+ and CD8+ T cells expressing IFNγ following exposure to autologous tumor lysate. The effect of vaccination on clinical markers of disease is being monitored.

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Matsushima, Hironori, Shuo Geng, Ran Lu, Takashi Okamoto, Yi Yao, Nobuyasu Mayuzumi, Paul F. Kotol, et al. "Neutrophil differentiation into a unique hybrid population exhibiting dual phenotype and functionality of neutrophils and dendritic cells." Blood 121, no. 10 (March 7, 2013): 1677–89. http://dx.doi.org/10.1182/blood-2012-07-445189.

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Key Points Both immature and mature neutrophils differentiate into a previously unrecognized hybrid population when cultured with GM-CSF. The resulting hybrids exhibit dual phenotype and functionality of both neutrophils and dendritic cells.

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40

Schierer, Stefan, Christian Ostalecki, Elisabeth Zinser, Ricarda Lamprecht, Bianca Plosnita, Lena Stich, Jan Dörrie, Manfred B. Lutz, Gerold Schuler, and Andreas S. Baur. "Extracellular vesicles from mature dendritic cells (DC) differentiate monocytes into immature DC." Life Science Alliance 1, no. 6 (December 2018): e201800093. http://dx.doi.org/10.26508/lsa.201800093.

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During inflammation, murine and human monocytes can develop into dendritic cells (DC), but this process is not entirely understood. Here, we demonstrate that extracellular vesicles (EV) secreted by mature human DC (maDC) differentiate peripheral monocytes into immature DC, expressing a unique marker pattern, including 6-sulfo LacNAc (slan), Zbtb46, CD64, and CD14. While EV from both maDC and immature DC differentiated monocytes similar to GM-CSF/IL-4 stimulation, only maDC-EV produced precursors, which upon maturation stimulus developed into T-cell–activating and IL-12p70–secreting maDC. Mechanistically, maDC-EV induced cell signaling through GM-CSF, which was abundant in EV as were IL-4 and other cytokines and chemokines. When injected into the mouse skin, murine maDC-EV attracted immune cells including monocytes that developed activation markers typical for inflammatory cells. Skin-injected EV also reached lymph nodes, causing a similar immune cell infiltration. We conclude that DC-derived EV likely serve to perpetuate an immune reaction and may contribute to chronic inflammation.

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Winzler, Claudia, Patrizia Rovere, Maria Rescigno, Francesca Granucci, Giuseppe Penna, Luciano Adorini, Valerie S. Zimmermann, Jean Davoust, and Paola Ricciardi-Castagnoli. "Maturation Stages of Mouse Dendritic Cells in Growth Factor–dependent Long-Term Cultures." Journal of Experimental Medicine 185, no. 2 (January 20, 1997): 317–28. http://dx.doi.org/10.1084/jem.185.2.317.

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The signals controlling the checkpoints of dendritic cells (DC) maturation and the correlation between phenotypical and functional maturational stages were investigated in a defined model system of growth factor–dependent immature mouse DC. Three sequential stages of DC maturation (immature, mature, and apoptotic) were defined and characterized. Immature DC (stage 1) had low expression of costimulatory molecules, highly organized cytoskeleton, focal adhesion plaques, and slow motility; accordingly, they were very efficient in antigen uptake and processing of soluble proteins. Further, at this stage most of major histocompatibility complex class II molecules were within cytoplasmic compartments consistent with a poor allostimulatory capacity. Bacteria or cytokines were very efficient in inducing progression from stage 1 towards stage 2 (mature). Morphological changes were observed by confocal analysis including depolymerization of F-actin and loss of vinculin containing adhesive structures which correlates with acquisition of high motility. Antigen uptake and presentation of native protein antigen was reduced. In contrast, presentation of immunogenic peptides and allostimulatory activity became very efficient and secretion of IL-12 p75 was detectable after antigen presentation. This functional DC maturation ended by apoptotic cell death, and no reversion to the immature phenotype was observed.

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Morva, Ahsen, Sébastien Lemoine, Achouak Achour, Jacques-Olivier Pers, Pierre Youinou, and Christophe Jamin. "Maturation and function of human dendritic cells are regulated by B lymphocytes." Blood 119, no. 1 (January 5, 2012): 106–14. http://dx.doi.org/10.1182/blood-2011-06-360768.

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Abstract Mature dendritic cells (DCs) are stimulators of T-cell immune response, whereas immature DCs support T-cell tolerance. Murine B cells can inhibit the production of IL-12 by DCs and thereby hinder the inflammatory response. Notwithstanding the importance of this modulation, only a few studies are available in humans. Here, we have developed an in vitro model of cocultures to assess its significance. We establish that human activated B cells restrained the development of monocytes into immature DCs and their differentiation into mature DCs. In addition, they decreased the density of HLA-DR from mature DCs, the expression of CD80 and CD86 coactivation molecules, the production of IL-12p70 required for antigen presentation and Th1 differentiation, and inhibited the DC-induced T-cell proliferation. These modulations were mediated by CD19+IgDlowCD38+CD24lowCD27− B cells and needed direct cell-to-cell contacts that involved CD62L for the control of CD80 and CD86 expression and a soluble factor for the control of IL-12 production. Moreover, mature DCs from patients with systemic lupus erythematosus displayed insensitivity to the regulation of IL-12. Overall, it appears that human B cells can regulate DC maturation and function and that inefficient B-cell regulation may influence an improper balance between an effector inflammatory response and tolerance induction.

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Kaliński, Paweł, Joost H. N. Schuitemaker, Catharien M. U. Hilkens, and Martien L. Kapsenberg. "Prostaglandin E2 Induces the Final Maturation of IL-12-Deficient CD1a+CD83+ Dendritic Cells: The Levels of IL-12 Are Determined During the Final Dendritic Cell Maturation and Are Resistant to Further Modulation." Journal of Immunology 161, no. 6 (September 15, 1998): 2804–9. http://dx.doi.org/10.4049/jimmunol.161.6.2804.

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Abstract Activation of immature dendritic cells (DC) in peripheral tissues induces their migration to lymph nodes and their maturation into CD83+ DC, which are able to prime naive T cells. The inflammatory cytokines IL-1β and TNF-α induce mature DC, which can secrete IL-12 and promote the development of Th0/Th1-biased cells. DC maturation factors with a Th2-promoting function have not been described. Here we show that PGE2, although it does not induce final DC maturation by itself, synergizes with IL-1β and TNF-α, and allows their effectiveness at 100-fold lower concentrations. While being phenotypically identical with the DC matured in the presence of high concentrations of IL-1β and TNF-α alone, DC matured in the additional presence of PGE2 show impaired IL-12 production and bias naive Th cell development toward the Th2. The ability of DC to produce IL-12 is also suppressed by IL-10, which in contrast to PGE2, inhibits their maturation. The differences in the ability to produce IL-12, established during the final DC maturation, are stable after the removal of modulatory factors. Importantly, fully mature DC become unsusceptible to PGE2 and IL-10. This indicates that the levels of IL-12 production in vivo, in mature DC interacting with Th cells within the lymph nodes, are mainly predetermined at the stage of immature DC in peripheral tissues. These data imply that the character of pathogen-induced local inflammatory reaction can “instruct” local DC to initiate Th1 or Th2-biased responses.

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Raftery, Martin J., Annette A. Kraus, Rainer Ulrich, Detlev H. Krüger, and Günther Schönrich. "Hantavirus Infection of Dendritic Cells." Journal of Virology 76, no. 21 (November 1, 2002): 10724–33. http://dx.doi.org/10.1128/jvi.76.21.10724-10733.2002.

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ABSTRACT Dendritic cells (DCs) play a pivotal role as antigen-presenting cells in the antiviral immune response. Here we show that Hantaan virus (HTNV), which belongs to the Bunyaviridae family (genus Hantavirus) and causes hemorrhagic fever with renal syndrome, productively infects human DCs in vitro. In the course of HTNV infection, DCs did not show any cytopathic effect and viral replication did not induce cell lysis or apoptosis. Furthermore, HTNV did not affect apoptosis-inducing signals that are important for the homeostatic control of mature DCs. In contrast to immunosuppressive viruses, e.g., human cytomegalovirus, HTNV activated immature DCs, resulting in upregulation of major histocompatibility complex (MHC), costimulatory, and adhesion molecules. Intriguingly, strong upregulation of MHC class I molecules and an increased intercellular cell adhesion molecule type 1 expression was also detected on HTNV-infected endothelial cells. In addition, antigen uptake by HTNV-infected DCs was reduced, another characteristic feature of DC maturation. Consistent with these findings, we observed that HTNV-infected DCs stimulated T cells as efficiently as did mature DCs. Finally, infection of DCs with HTNV induced the release of the proinflammatory cytokines tumor necrosis factor alpha and alpha interferon. Taken together, our findings indicate that hantavirus-infected DCs may significantly contribute to hantavirus-associated pathogenesis.

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Zhukov, A. S., I. E. Belousova, V. R. Khairutdinov, and A. V. Samtsov. "Role of langerin-positive and CD83+ cells in the pathogenesis of mycosis fungoides." Vestnik dermatologii i venerologii 89, no. 4 (August 15, 2013): 38–43. http://dx.doi.org/10.25208/vdv602.

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Dendritic cells regulate the balance between the immune response and immunotolerance; their role in the pathogenesis of skin lymphomas is underexplored. Goal. To study the number of populations of CD83+ and langerin positive cells in the skin of patients suffering from mycosis fungoides and small plaque parapsoriasis. Materials and methods. The authors determined the content of langerin-positive and CD83+ cells by means of immunohistochemistry of skin biopsy samples taken from patients suffering from mycosis fungoides (17 subjects) and small plaque parapsoriasis (6 subjects). The control group comprised 16 healthy people. Results. The study revealed that langerin positive and CD83+ dendritic cells prevailed in patients suffering from mycosis fungoides as compared to patients with small plaque parapsoriasis and healthy subjects. The share of immature dendritic cells grows in patients with parapsoriasis and mycosis fungoides. Conclusion. The statistically reliable difference between the amount of langerin positive and CD83+ dendritic cells as well as immature to mature dendritic cells ratio in case of mycosis fungoides vs. small plaque parapsoriasis can serve as an additional diagnostics criterion for these diseases.

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Coronel, Roxanne, Sachiko Takayama, Timothy Juwono, and Laura Hertel. "Dynamics of Human Cytomegalovirus Infection in CD34+Hematopoietic Cells and Derived Langerhans-Type Dendritic Cells." Journal of Virology 89, no. 10 (March 11, 2015): 5615–32. http://dx.doi.org/10.1128/jvi.00305-15.

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ABSTRACTAcquisition of human cytomegalovirus (CMV) usually occurs by contact between contaminated bodily fluids, such as urine and saliva, and host mucosal cells. Langerhans-type dendritic cells (LC) are the only type of immune cells found in the outermost layers of the oral mucosae, where they not only provide a first line of defense against CMV but can easily be targeted by orally administered vaccines, while their bone marrow resident progenitors are important sites of virus latency. In this work, we tracked the progress of infection in CD34+progenitor cells, immature LC (iLC), and mature LC (mLC) exposed to the clinical-like strain TB40-BAC4 or to the vaccine strain AD169varATCC, prior to their long-term maintenance under either immature or mature conditions. We show that the genomes of both strains are efficiently maintained in CD34+cells during their differentiation into iLC, although this requires the presence of larger amounts of input AD169varATCC DNA. Lipopolysaccharide- and CD40 ligand-induced maturation of iLC derived from latently infected progenitors was not associated with robust viral genome replication and progeny production, while maturation of directly infected iLC increased and prolonged expression of the viral immediate early proteins. While effective replication of viral genomes from both strains occurred only in mLC, both iLC and mLC produced viral progeny, suggesting that both types of LC may contribute to CMV horizontal transmissionin vivo.IMPORTANCEHuman CMV is usually acquired via the oral and nasal mucosae. Langerhans-type dendritic cells (LC) are the only type of immune cells found in the outermost layers of these tissues. Understanding how CMV interacts with LC and their hematopoietic progenitors is thus essential to develop innovative means of defense against this virus. Here we show that the genomes of a virulent and an attenuated strain of CMV are maintained in hematopoietic progenitor cells during their differentiation into immature LC and that maturation of these cells by exposure to lipopolysaccharide and CD40 ligand is not sufficient to trigger virus reactivation. While the extents of viral protein expression and genome replication were broadest in directly infected mature LC populations, similar amounts of viral progeny were detected in the supernatants of immature and mature LC, suggesting that these immune cells of the oral mucosa are likely to be important for CMV transmission within the human population.

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Lechmann, Matthias, Daniëlle J. E. B. Krooshoop, Diana Dudziak, Elisabeth Kremmer, Christine Kuhnt, Carl G. Figdor, Gerold Schuler, and Alexander Steinkasserer. "The Extracellular Domain of CD83 Inhibits Dendritic Cell–mediated T Cell Stimulation and Binds to a Ligand on Dendritic Cells." Journal of Experimental Medicine 194, no. 12 (December 17, 2001): 1813–21. http://dx.doi.org/10.1084/jem.194.12.1813.

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CD83 is an immunoglobulin (Ig) superfamily member that is upregulated during the maturation of dendritic cells (DCs). It has been widely used as a marker for mature DCs, but its function is still unknown. To approach its potential functional role, we have expressed the extracellular Ig domain of human CD83 (hCD83ext) as a soluble protein. Using this tool we could show that immature as well as mature DCs bind to CD83. Since CD83 binds a ligand also expressed on immature DCs, which do not express CD83, indicates that binding is not a homophilic interaction. In addition we demonstrate that hCD83ext interferes with DC maturation downmodulating the expression of CD80 and CD83, while no phenotypical effects were observed on T cells. Finally, we show that hCD83ext inhibits DC-dependent allogeneic and peptide-specific T cell proliferation in a concentration dependent manner in vitro. This is the first report regarding functional aspects of CD83 and the binding of CD83 to DCs.

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CAO, Weiping, Szu Hee LEE, and Jinhua LU. "CD83 is preformed inside monocytes, macrophages and dendritic cells, but it is only stably expressed on activated dendritic cells." Biochemical Journal 385, no. 1 (December 14, 2004): 85–93. http://dx.doi.org/10.1042/bj20040741.

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Human DCs (dendritic cells) express surface CD83 upon activation. Comparing the surface induction of CD83 with the upregulation of CD40, CD80 and CD86 during LPS (lipopolysaccharide)-induced DC maturation showed that CD83 induction occurred more rapidly. Despite the lack of CD83 on immature DCs, it was detected in these cells by Western blotting and flow cytometry. Indirect immunofluorescence revealed CD83 inside immature DCs in perinuclear regions. CD83 was absent on monocytes and macrophages, but it was detected inside these cells and found to be rapidly surface-expressed upon LPS-induced activation. Whereas CD83 expression on activated DCs was sustainable, its expression on monocytes and macrophages was transient. Optimal interleukin-4 co-stimulation during DC generation from monocytes was found to be essential for stable CD83 surface expression. CD83 was detected as 37 and 50 kDa forms in transfected 293T cells. Macrophages and immature DCs expressed the 37 kDa form, whereas mature DCs predominantly expressed the 50 kDa form. In monocytes, CD83 was detected as a 22 kDa detergent-insoluble form. The rapid CD83 surface induction on DCs and macrophages was blocked by brefeldin A, but not by cycloheximide, showing that fresh CD83 synthesis was not essential. Tunicamycin inhibited the expression of the 50 and 37 kDa CD83 forms, and also blocked CD83 surface expression on DCs and macrophages. PNGase F (peptide N-glycosidase F) digestion reduced the 37 and 50 kDa CD83 forms to 28 kDa. In summary, monocytes, macrophages and immature DCs contain preformed intracellular CD83, and its rapid surface expression upon activation is post-translationally regulated in a process involving glycosylation.

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Cignetti, Alessandro, Antonella Vallario, Ilaria Roato, Paola Circosta, Bernardino Allione, Laura Casorzo, Paolo Ghia, and Federico Caligaris-Cappio. "Leukemia-Derived Immature Dendritic Cells Differentiate into Functionally Competent Mature Dendritic Cells That Efficiently Stimulate T Cell Responses." Journal of Immunology 173, no. 4 (August 4, 2004): 2855–65. http://dx.doi.org/10.4049/jimmunol.173.4.2855.

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Geissmann, Frederic, Yves Lepelletier, Sylvie Fraitag, Jenny Valladeau, Christine Bodemer, Marianne Debré, Michelle Leborgne, Sem Saeland, and Nicole Brousse. "Differentiation of Langerhans cells in Langerhans cell histiocytosis." Blood 97, no. 5 (March 1, 2001): 1241–48. http://dx.doi.org/10.1182/blood.v97.5.1241.

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Langerhans cell histiocytosis (LCH) consists of lesions composed of cells with a dendritic Langerhans cell (LC) phenotype. The clinical course of LCH ranges from spontaneous resolution to a chronic and sometimes lethal disease. We studied 25 patients with various clinical forms of the disease. In bone and chronic lesions, LCH cells had immature phenotype and function. They coexpressed LC antigens CD1a and Langerin together with monocyte antigens CD68 and CD14. Class II antigens were intracellular and LCH cells almost never expressed CD83 or CD86 or dendritic cell (DC)–Lamp, despite their CD40 expression. Consistently, LCH cells sorted from bone lesions (eosinophilic granuloma) poorly stimulated allogeneic T-cell proliferation in vitro. Strikingly, however, in vitro treatment with CD40L induced the expression of membrane class II and CD86 and strongly increased LCH cell allostimulatory activity to a level similar to that of mature DCs. Numerous interleukin-10–positive (IL-10+), Langerin−, and CD68+ macrophages were found within bone and lymph node lesions. In patients with self-healing and/or isolated cutaneous disease, LCH cells had a more mature phenotype. LCH cells were frequently CD14− and CD86+, and macrophages were rare or absent, as were IL-10–expressing cells. We conclude that LCH cells in the bone and/or chronic forms of the disease accumulate within the tissues in an immature state and that most probably result from extrinsic signals and may be induced to differentiate toward mature DCs after CD40 triggering. Drugs that enhance the in vivo maturation of these immature DCs, or that induce their death, may be of therapeutic benefit.

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

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