scholarly journals Plasmacytoid dendritic cells inhibit pulmonary immunopathology and promote clearance of respiratory syncytial virus

2006 ◽  
Vol 203 (5) ◽  
pp. 1153-1159 ◽  
Author(s):  
Joost J. Smit ◽  
Brian D. Rudd ◽  
Nicholas W. Lukacs
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Dendritic Cell ◽  
Immune Responses ◽  
Plasmacytoid Dendritic Cell ◽  
Protective Role ◽  
Plasmacytoid Dendritic Cells ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Acquired Immune Responses

Respiratory syncytial virus (RSV) infection is widely spread and is a major cause of bronchiolitis in infants and high-risk adults, often leading to hospitalization. RSV infection leads to obstruction and inflammation of the airways and induction of innate and acquired immune responses. Because dendritic cells (DCs) are essential in the elicitation of these immune responses, we investigated the presence and the role of dendritic cell subtypes upon RSV infection in the lung. Here, we report that RSV infection increased the number of both conventional and plasmacytoid dendritic cells in the lung and the lung-draining lymph nodes. In particular, the increase in plasmacytoid dendritic cell numbers was sustained and lasted until 30 d after infection. Depletion of plasmacytoid dendritic cells resulted in decreased RSV clearance. In addition, depletion of plasmacytoid dendritic cells resulted in an exacerbation of all manifestations of immune-mediated pathology caused by RSV infection. In conclusion, this study demonstrates that both conventional and plasmacytoid dendritic cells are attracted to the site of RSV infection. It is demonstrated that plasmacytoid dendritic cells play a protective role during RSV infection by modulation of local immune responses.

scholarly journals Plasmacytoid Dendritic Cells Contribute to the Production of IFN-β via TLR7-MyD88-Dependent Pathway and CTL Priming during Respiratory Syncytial Virus Infection

Viruses ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 730 ◽  
Author(s):  
Tae Hoon Kim ◽  
Dong Sun Oh ◽  
Hi Eun Jung ◽  
Jun Chang ◽  
Heung Kyu Lee
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Type I Interferon ◽  
Yellow Fluorescent Protein ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Antigen Specificity ◽  
Interferon Β ◽  
Rsv Infection ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) is the leading cause of respiratory viral infection in infants and children, yet little is known about the antiviral response of plasmacytoid dendritic cells (pDCs) to RSV infection. We tracked the cellular source of interferon-β using interferon-β/yellow fluorescent protein (YFP) reporter mice and identified the signaling pathway activated by RSV that induces type I interferon production in pDCs and DCs. Results from in vitro analyses of RSV-stimulated bone marrow cells revealed that RSV induces interferon-β production in both pDCs and DCs. Kinetic analyses of interferon-β-producing cells in RSV-infected lung cells in vivo indicated that pDCs are rapidly recruited to sites of inflammation during infection. These cells produced interferon-β via the TLR7-MyD88-mediated pathway and IFNα1R-mediated pathway rather than the MAVS-mediated pathway. Moreover, pDC-ablated mice exhibited decreased interferon-γ production and the antigen specificity of CD8+ T cells. Collectively, these data indicate that pDCs play pivotal roles in cytotoxic T lymphocyte (CTL) responses and are one of producers of type I interferon during RSV infection.

scholarly journals Contribution of Dendritic Cells in Protective Immunity against Respiratory Syncytial Virus Infection

Viruses ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 102 ◽  
Author(s):  
Hi Eun Jung ◽  
Tae Hoon Kim ◽  
Heung Kyu Lee
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Immune Responses ◽  
Defense Mechanisms ◽  
Adaptive Immune Response ◽  
The Elderly ◽  
Effective Vaccine ◽  
Adaptive Immune ◽  
Rsv Infection ◽  
Syncytial Virus

Respiratory syncytial virus (RSV) is a major cause of severe respiratory disease in infants and the elderly. The socioeconomic burden of RSV infection is substantial because it leads to serious respiratory problems, subsequent hospitalization, and mortality. Despite its clinical significance, a safe and effective vaccine is not yet available to prevent RSV infection. Upon RSV infection, lung dendritic cells (DCs) detecting pathogens migrate to the lymph nodes and activate the adaptive immune response. Therefore, RSV has evolved various immunomodulatory strategies to inhibit DC function. Due to the capacity of RSV to modulate defense mechanisms in hosts, RSV infection results in inappropriate activation of immune responses resulting in immunopathology and frequent reinfection throughout life. This review discusses how DCs recognize invading RSV and induce adaptive immune responses, as well as the regulatory mechanisms mediated by RSV to disrupt DC functions and ultimately avoid host defenses.

scholarly journals Inhibition of Toll-Like Receptor 7- and 9-Mediated Alpha/Beta Interferon Production in Human Plasmacytoid Dendritic Cells by Respiratory Syncytial Virus and Measles Virus

2005 ◽  
Vol 79 (9) ◽  
pp. 5507-5515 ◽  
Author(s):  
Jörg Schlender ◽  
Veit Hornung ◽  
Stefan Finke ◽  
Margit Günthner-Biller ◽  
Sabrina Marozin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Immune Responses ◽  
Measles Virus ◽  
Plasmacytoid Dendritic Cells ◽  
Toll Like Receptor ◽  
Beta Interferon ◽  
Cpg Oligodeoxynucleotide ◽  
Alpha Beta ◽  
Syncytial Virus

ABSTRACT Human plasmacytoid dendritic cells (PDC) are key sentinels alerting both innate and adaptive immune responses through production of huge amounts of alpha/beta interferon (IFN). IFN induction in PDC is triggered by outside-in signal transduction pathways through Toll-like receptor 7 (TLR7) and TLR9 as well as by recognition of cytosolic virus-specific patterns. TLR7 and TLR9 ligands include single-stranded RNA and CpG-rich DNA, respectively, as well as synthetic derivatives thereof which are being evaluated as therapeutic immune modulators promoting Th1 immune responses. Here, we identify the first viruses able to block IFN production by PDC. Both TLR-dependent and -independent IFN responses are abolished in human PDC infected with clinical isolates of respiratory syncytial virus (RSV), RSV strain A2, and measles virus Schwarz, in contrast to RSV strain Long, which we previously identified as a potent IFN inducer in human PDC (Hornung et al., J. Immunol. 173:5935-5943, 2004). Notably, IFN synthesis of PDC activated by the TLR7 and TLR9 agonists resiquimod (R848) and CpG oligodeoxynucleotide 2216 is switched off by subsequent infection by RSV A2 and measles virus. The capacity of RSV and measles virus of human PDC to shut down IFN production should contribute to the characteristic features of these viruses, such as Th2-biased immune pathology, immune suppression, and superinfection.

scholarly journals Sirtuin 1 Regulates Dendritic Cell Activation and Autophagy during Respiratory Syncytial Virus–Induced Immune Responses

2015 ◽  
Vol 195 (4) ◽  
pp. 1637-1646 ◽  
Author(s):  
Anna B. Owczarczyk ◽  
Matthew A. Schaller ◽  
Michelle Reed ◽  
Andrew J. Rasky ◽  
David B. Lombard ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Dendritic Cell ◽  
Immune Responses ◽  
Cell Activation ◽  
Sirtuin 1 ◽  
Dendritic Cell Activation ◽  
Syncytial Virus

scholarly journals The Role of Toll-like receptor 4 in respiratory syncytial virus replication, interferon lambda 1 induction, and chemokine responses

2018 ◽  
Author(s):  
Lindsay Broadbent ◽  
Jonathon D. Coey ◽  
Michael D. Shields ◽  
Ultan F. Power
Keyword(s):  
Respiratory Syncytial Virus ◽  
Immune Responses ◽  
P38 Mapk ◽  
Inflammatory Cytokines ◽  
Virus Replication ◽  
Growth Kinetics ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Pro Inflammatory Cytokines

AbstractRespiratory syncytial virus (RSV) infection is the leading cause of severe lower respiratory tract infections (LRTI) in infants worldwide. The immune responses to RSV infection are implicated in RSV pathogenesis but RSV immunopathogenesis in humans remains poorly understood. We previously demonstrated that IFN-λ1 is the principle interferon induced following RSV infection of infants and well-differentiated primary pediatric bronchial epithelial cells (WD-PBECs). Interestingly, RSV F interacts with the TLR4/CD14/MD2 complex to initiate secretion of pro-inflammatory cytokines, while TLR4 stimulation with house dust mite induces IFN-λ1 production. However, the role of TLR4 in RSV infection and concomitant IFN-λ1 induction remains unclear. Using our RSV/WD-PBEC infection model, we found that CLI-095 inhibition of TLR4 resulted in significantly reduced viral growth kinetics, and secretion of IFN-λ1 and pro-inflammatory chemokines. To elucidate specific TLR4 signalling intermediates implicated in virus replication and innate immune responses we selected 4 inhibitors, including LY294002, U0126, SB203580 and JSH-23. SB203580, a p38 MAPK inhibitor, reduced both viral growth kinetics and IFN-λ1 secretion, while JSH-23, an NF-κB inhibitor, reduced IFN-λ1 secretion without affecting virus growth kinetics. Our data indicate that TLR4 plays a role in RSV entry and/or replication and IFN-λ1 induction following RSV infection is mediated, in part, by TLR4 signalling through NF- κB and/or p38 MAPK. Therefore, targeting TLR4 or downstream effector proteins could present novel treatment strategies against RSV.ImportanceThe role of TLR4 in RSV infection and IFN-λ1 induction is controversial. Using our WD-PBEC model, which replicates many hallmarks of RSV infection in vivo, we demonstrated that the TLR4 pathway is involved in both RSV infection and/or replication and the concomitant induction of IFN-λ1 and other pro-inflammatory cytokines. Increasing our understanding of the role of TLR4 in RSV immunopathogenesis may lead to the development of novel RSV therapeutics.

SPIB, a novel immunohistochemical marker for human blastic plasmacytoid dendritic cell neoplasms: characterization of its expression in major hematolymphoid neoplasms

Blood ◽  
2013 ◽  
Vol 121 (4) ◽  
pp. 643-647 ◽  
Author(s):  
Santiago Montes-Moreno ◽  
Rocio Ramos-Medina ◽  
Azahara Martínez-López ◽  
Carlos Barrionuevo Cornejo ◽  
Alejandro Parra Cubillos ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Transcription Factor ◽  
T Cell ◽  
Dendritic Cell ◽  
Cell Lymphoma ◽  
Plasmacytoid Dendritic Cell ◽  
Plasmacytoid Dendritic Cells ◽  
Ets Transcription Factor ◽  
Hematolymphoid Neoplasms

Abstract SPIB is an Ets transcription factor that is expressed exclusively in mature B cells, T-cell progenitors, and plasmacytoid dendritic cells. In the present study, we developed a novel mAb against the SPIB protein and characterized its expression in major hematolymphoid neoplasms, including a series of 45 cases of blastic plasmacytoid dendritic cell (BPDC) neoplasms and their potential cutaneous mimics. We found that SPIB is expressed heterogeneously among B- and T-cell lymphoma types. Interestingly, SPIB is expressed in a large proportion of nongerminal center type DLBCLs. In cutaneous neoplasms, SPIB is overexpressed in all BPDC neoplasms, but none of its cutaneous mimics. SPIB remains overexpressed in all cases that lack 1 or 2 of the markers used for BPDC neoplasms (ie, CD4, CD56, TCL1, and CD123). We conclude that SPIB expression can be used as a tool for diagnosing BPDC neoplasms, but it needs to be tested in conjunction with the growing arsenal of markers for human plasmacytoid dendritic cells.

scholarly journals Respiratory syncytial virus differentially activates murine myeloid and plasmacytoid dendritic cells

Immunology ◽  
2007 ◽  
Vol 122 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Ivette Boogaard ◽  
Marijke van Oosten ◽  
Leonie S. van Rijt ◽  
Femke Muskens ◽  
Tjeerd G. Kimman ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Plasmacytoid Dendritic Cells ◽  
Syncytial Virus
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