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Dendritic Cell Activation (dendritic + cell_activation)
Selected AbstractsDendritic cell activation by combined exposure to anti-CD40 plus interleukin (IL)-12 and IL-18 efficiently stimulates anti-tumor immunityEXPERIMENTAL DERMATOLOGY, Issue 1 2009Sandra Balkow Abstract:, Despite as yet limited clinical effectiveness, dendritic cell (DC)-based immunotherapy remains a promising approach for the treatment of cancer, but requires further improvement in its immunostimulatory effectiveness. Potent anti-tumor immunity often depends on the induction of type 1 (TH1) immune responses. Therefore, we combined different DC maturation stimuli that are known to induce TH1 immunity [anti-CD40, interleukin (IL)-12, IL-18], with the aim to trigger a TH1 driven anti-tumor CTL response. When compared with untreated DC or DC treated with anti-CD40 alone, DC matured with anti-CD40 plus IL-12 and IL-18 expressed significantly more IFN-, and IL-12, induced enhanced CD8+ T-cell proliferation, prolonged synaptic interaction with T cells and increased CD8+ T-cell-mediated cytotoxicity. To analyse if these DC are able to induce efficient anti-tumor immunity, mice carrying a B16-OVA tumor were treated with tumor antigen (TA)-loaded DC that had been exposed to anti-CD40 or to anti-CD40 plus IL-12 and IL-18. Our data show that anti-CD40 plus IL-12 and IL-18 matured DC are superior to controls in retarding tumor growth. These data indicate that maturation of DC with anti-CD40 plus IL-12 and IL-18 potently stimulates the generation of an anti-tumor immune response and may lead to improved immunotherapeutic capacity of DC vaccination. [source] Dendritic cell activation by danger and antigen-specific T-cell signallingEXPERIMENTAL DERMATOLOGY, Issue 5 2000A. D. McLellan Abstract: Recent transplantation, animal and in vitro studies suggest a dependence of some immune reactions on tissue damage. Although many factors involved in enhancing immune responses through tissue damage have yet to be identified, recent data suggests that one of the targets of these cellular stress factors is the bone marrow derived dendritic cell ( DC). DC are potent initiators of primary immune responses and hold the key to immune reactions through their ability to sense changes in their local environment and respond appropriately to induce T-cell immunity, or possibly tolerance. In the lymph node, DC are also influenced by antigen-specific signalling from T cells, which may extend and amplify DC antigen presenting capabilities, especially for the stimulation of cytotoxic responses. It now appears that both tissue damage and antigen-specific T-cell derived signals act together on the DC to promote the appropriate immune reaction to antigen. Thus DC antigen presenting behaviour is not only dependent on the context of antigen encounter in the periphery, but also on the availability of antigen-specific T cells and their T-cell receptor specificities. [source] New concepts in antimalarial use and mode of action in dermatologyDERMATOLOGIC THERAPY, Issue 4 2007Sunil Kalia ABSTRACT: Although chloroquine, hydroxychloroquine and quinacrine were originally developed for the treatment of malaria, these medications have been used to treat skin disease for over 50 years. Recent clinical data have confirmed the usefulness of these medications for the treatment of lupus erythematosus. Current research has further enhanced our understanding of the pharmacologic mechanisms of action of these drugs involving inhibition of endosomal toll-like receptor (TLR) signaling limiting B cell and dendritic cell activation. With this understanding, the use of these medications in dermatology is broadening. This article highlights the different antimalarials used within dermatology through their pharmacologic properties and mechanism of action, as well as indicating their clinical uses. In addition, contraindications, adverse effects, and possible drug interactions of antimalarials are reviewed. [source] Plasmacytoid dendritic cell activation by foot-and-mouth disease virus requires immune complexesEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2006Laurence Guzylack-Piriou Abstract Natural IFN-producing cells (NIPC), also called plasmacytoid dendritic cells, represent an essential component of the innate immune defense against infection. Despite this, not much is known about the pathways involved in their activation by non-enveloped viruses. The present study demonstrates that the non-enveloped foot-and-mouth disease virus (FMDV) cannot stimulate IFN-, responses in NIPC, unless complexed with FMDV-specific immunoglobulins. Stimulation of NIPC with such immune complexes employs Fc,RII ligation, leading to strong secretion of IFN-,. In contrast to the stimulation of NIPC by many enveloped viruses, FMDV induction of IFN-, production requires live virus. It is necessary for the virus to initiate its replicative cycle. Moreover, it is an abortive replication, as witnessed by the decrease of dsRNA levels and viral titers with time post infection. Sensitivity of the NIPC stimulation to wortmannin and chloroquin, but not leupeptin, indicates an essential role for the pre-lysosomal stage endosomal compartment. In conclusion, the present study demonstrates that immune complexes provide the means for a non-interferogenic virus to induce IFN-, responses by NIPC. This indicates an important link between NIPC and antibodies in immune responses against non-enveloped viruses such as FMDV. [source] LIGHTing up dendritic cell activation: Immune regulation and viral exploitationJOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2005Gabriele Pollara The maturation state of dendritic cells (DC) is regulated by a variety of factors. These include ligands expressed by T cells, such as members of the TNF superfamily. Recent studies have highlighted the role of one such molecule, LIGHT, as a positive regulator of DC biology, promoting the maturation of these cells through the activation of NF-,B pathways. In addition, HSV-1 envelope glycoproteins can also bind the LIGHT receptor, herpes virus entry mediator (HVEM), and activate similar downstream signalling pathways in DC. The consequence of this host-viral interaction may be a novel pathway of viral immune evasion. © 2005 Wiley-Liss, Inc. [source] Filaria/Wolbachia activation of dendritic cells and development of Th1-associated responses is dependent on Toll-like receptor 2 in a mouse model of ocular onchocerciasis (river blindness)PARASITE IMMUNOLOGY, Issue 9 2007K. DAEHNEL SUMMARY Toll-like receptors (TLRs) regulate dendritic cell function and activate signals that mediate the nature of the adaptive immune response. The current study examined the role of TLRs in dendritic cell activation and in regulating T cell and antibody responses to antigens from the filarial parasites Onchocerca volvulus and Brugia malayi, which cause river blindness and lymphatic filariasis, respectively. Bone-marrow-derived CD11c+ cells from C57BL/6 and TLR4,/, mice produced high levels of IL-6 and RANTES, and showed elevated surface CD40 expression, whereas CD11c+ cells from myeloid differentiation factor 88,/, (MyD88,/,), TLR2,/, and TLR2/4,/, mice were not activated. Similarly, IFN-, production by splenocytes from immunized TLR2,/, mice was significantly impaired compared with splenocytes from C57BL/6 and TLR4,/, mice. In contrast, there was no difference among these strains in Th2-associated responses including IL-5 production by splenocytes from immunized animals, serum IgE and IgG1, or eosinophil infiltration into the corneal stroma. Neutrophil recruitment to the cornea and CXC chemokine production was inhibited in immunized TLR2,/, mice compared with C57BL/6 and TLR4,/, mice. Taken together, these findings demonstrate an essential role for TLR2 in filaria-induced dendritic cell activation, IFN-, production and neutrophil migration to the cornea, but does not affect filaria-induced Th2-associated responses. [source] Surfactant protein D inhibits mite-induced alveolar macrophage and dendritic cell activations through TLR signalling and DC-SIGN expressionCLINICAL & EXPERIMENTAL ALLERGY, Issue 1 2010C-F Liu Summary Background Surfactant protein D (SP-D), a secreted pattern recognition molecule associated with pulmonary innate immunity, has been shown to mediate the clearance of pathogens in multiple ways. However, how SP-D interacts with alveolar macrophages (AMs) and dendritic cells (DCs) during allergen exposure remains unclear. Objective This study was performed to characterize the immunomodulatory effects of SP-D on mite allergen (Dermatophagoides pteronyssinus, Der p)-induced inflammatory signalling in AMs and DCs. Methods Murine AM, alveolar macrophage cell line derived from BALB/c mice (MH-S cells), and human monocyte-derived dendritic cells (MDDC) were used as model systems. The production of nitric oxide (NO) and TNF-,, expression of surface Toll-like receptors (TLRs), and expression of the C-type lectin receptor known as dendritic cell (DC)-specific ICAM-grabbing non-integrin (DC-SIGN) were measured as a function of pretreatment with SP-D and subsequent exposure to Der p. Der p-dependent cellular activations that were modified by SP-D in these model systems were then identified. Results Pretreatment of MH-S cells with SP-D reduced Der p-dependent production of NO, TNF-,, and the downstream activations of IL-1 receptor-associated kinase, mitogen activated protein kinase (MAPK) kinase, and nuclear factor-,B. SP-D interacted with CD14 such that CD14 binding to Der p was inhibited and Der p-induced signalling via TLRs was blocked. DC-SIGN expression was suppressed by Der p in MH-S and MDDC; this down-regulation of DC-SIGN expression was prevented by pretreatment with SP-D. Conclusions These results indicated that the inhibition of Der p-induced activation of MH-S and MDDC by SP-D is mediated through suppression of the CD14/TLR signalling pathway and maintenance of DC-SIGN expression, which may protect allergen-induced airway inflammation. Cite this as: C-F Liu, M. Rivere, H-J Huang, G. Puzo and J-Y Wang, Clinical & Experimental Allergy, 2010 (40) 111,122. [source] | ||||||||||||||||||||||