scholarly journals IRF-3, IRF-5, and IRF-7 Coordinately Regulate the Type I IFN Response in Myeloid Dendritic Cells Downstream of MAVS Signaling

2013 ◽  
Vol 9 (1) ◽  
pp. e1003118 ◽  
Author(s):  
Helen M. Lazear ◽  
Alissa Lancaster ◽  
Courtney Wilkins ◽  
Mehul S. Suthar ◽  
Albert Huang ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Type I ◽  
Type I Ifn ◽  
Myeloid Dendritic Cells

scholarly journals Correction: IRF-3, IRF-5, and IRF-7 Coordinately Regulate the Type I IFN Response in Myeloid Dendritic Cells Downstream of MAVS Signaling

2013 ◽  
Vol 9 (5) ◽  
Author(s):  
Helen M. Lazear ◽  
Alissa Lancaster ◽  
Courtney Wilkins ◽  
Mehul S. Suthar ◽  
Albert Huang ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Type I ◽  
Type I Ifn ◽  
Myeloid Dendritic Cells

scholarly journals Differential Induction of Type I Interferon Responses in Myeloid Dendritic Cells by Mosquito and Mammalian-Cell-Derived Alphaviruses

2006 ◽  
Vol 81 (1) ◽  
pp. 237-247 ◽  
Author(s):  
Reed S. Shabman ◽  
Thomas E. Morrison ◽  
Christopher Moore ◽  
Laura White ◽  
Mehul S. Suthar ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Mammalian Cell ◽  
Mammalian Cells ◽  
Type I Interferon ◽  
Mosquito Cell ◽  
Type I ◽  
Mosquito Vector ◽  
Type I Ifn ◽  
Myeloid Dendritic Cells ◽  
Equine Encephalitis Virus

ABSTRACT Dendritic cells (DCs) are an important early target cell for many mosquito-borne viruses, and in many cases mosquito-cell-derived arboviruses more efficiently infect DCs than viruses derived from mammalian cells. However, whether mosquito-cell-derived viruses differ from mammalian-cell-derived viruses in their ability to induce antiviral responses in the infected dendritic cell has not been evaluated. In this report, alphaviruses, which are mosquito-borne viruses that cause diseases ranging from encephalitis to arthritis, were used to determine whether viruses grown in mosquito cells differed from mammalian-cell-derived viruses in their ability to induce type I interferon (IFN) responses in infected primary dendritic cells. Consistent with previous results, mosquito-cell-derived Ross River virus (mos-RRV) and Venezuelan equine encephalitis virus (mos-VEE) exhibited enhanced infection of primary myeloid dendritic cells (mDCs) compared to mammalian-cell-derived virus preparations. However, unlike the mammalian-cell-derived viruses, which induced high levels of type I IFN in the infected mDC cultures, mos-RRV and mos-VEE were poor IFN inducers. Furthermore, the poor IFN induction by mos-RRV contributed to the enhanced infection of mDCs by mos-RRV. These results suggest that the viruses initially delivered by the mosquito vector differ from those generated in subsequent rounds of replication in the host, not just with respect to their ability to infect dendritic cells but also in their ability to induce or inhibit antiviral type I IFN responses. This difference may have an important impact on the mosquito-borne virus's ability to successfully make the transition from the arthropod vector to the vertebrate host.

scholarly journals Type I Interferon Released by Myeloid Dendritic Cells Reversibly Impairs Cytomegalovirus Replication by Inhibiting Immediate Early Gene Expression

2015 ◽  
Vol 89 (19) ◽  
pp. 9886-9895 ◽  
Author(s):  
Julia Katharina Holzki ◽  
Franziska Dağ ◽  
Iryna Dekhtiarenko ◽  
Ulfert Rand ◽  
Rosaely Casalegno-Garduño ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Dendritic Cells ◽  
Viral Latency ◽  
Immediate Early ◽  
Type I ◽  
Type I Ifn ◽  
Myeloid Dendritic Cells

ABSTRACTCytomegalovirus (CMV) is a ubiquitous beta-herpesvirus whose reactivation from latency is a major cause of morbidity and mortality in immunocompromised hosts. Mouse CMV (MCMV) is a well-established model virus to study virus-host interactions. We showed in this study that the CD8-independent antiviral function of myeloid dendritic cells (mDC) is biologically relevant for the inhibition of MCMV replicationin vivoandin vitro. In vivoablation of CD11c+DC resulted in higher viral titers and increased susceptibility to MCMV infection in the first 3 days postinfection. We developedin vitrococulture systems in which we cocultivated MCMV-infected endothelial cells or fibroblasts with T cell subsets and/or dendritic cells. While CD8 T cells failed to control MCMV replication, bone marrow-derived mDC reduced viral titers by a factor of up to 10,000. Contact of mDC with the infected endothelial cells was crucial for their antiviral activity. Soluble factors secreted by the mDC blocked MCMV replication at the level of immediate early (IE) gene expression, yet the viral lytic cycle reinitiated once the mDC were removed from the cells. On the other hand, the mDC did not impair MCMV replication in cells deficient for the interferon (IFN) alpha/beta receptor (IFNAR), arguing that type I interferons were critical for viral control by mDC. In light of our recent observation that type I IFN is sufficient for the induction of latency immediately upon infection, our results imply that IFN secreted by mDC may play an important role in the establishment of CMV latency.IMPORTANCENumerous studies have focused on the infection of DC with cytomegaloviruses and on the establishment of latency within them. However, almost all of these studies have relied on the infection of DC monoculturesin vitro, whereas DC are just one among many cell types present in an infection sitein vivo. To mimic this aspect of thein vivosituation, we cocultured DC with infected endothelial cells or fibroblasts. Our data suggest that direct contact with virus-infected endothelial cells activates CD11c+DC, which leads to reversible suppression of MCMV replication at the level of IE gene expression by a mechanism that depends on type I IFN. The effect matches the formal definition of viral latency. Therefore, our data argue that the interplay of dendritic cells and infected neighboring cells might play an important role in the establishment of viral latency.

scholarly journals Rapid Differentiation of Monocytes into Type I IFN-Producing Myeloid Dendritic Cells as an Antiviral Strategy against Influenza Virus Infection

2012 ◽  
Vol 189 (5) ◽  
pp. 2257-2265 ◽  
Author(s):  
Weiping Cao ◽  
Andrew K. Taylor ◽  
Renata E. Biber ◽  
William G. Davis ◽  
Jin Hyang Kim ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Type I ◽  
Type I Ifn ◽  
Myeloid Dendritic Cells

scholarly journals A Type I IFN-Dependent Pathway Induced by Schistosoma mansoni Eggs in Mouse Myeloid Dendritic Cells Generates an Inflammatory Signature

2004 ◽  
Vol 172 (5) ◽  
pp. 3011-3017 ◽  
Author(s):  
François Trottein ◽  
Norman Pavelka ◽  
Caterina Vizzardelli ◽  
Veronique Angeli ◽  
Claudia S. Zouain ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Schistosoma Mansoni ◽  
Type I ◽  
Type I Ifn ◽  
Myeloid Dendritic Cells ◽  
Dependent Pathway

PLASMACYTOID DENDRITIC CELLS FUNCTION IN HIV INFECTION

2008 ◽  
Vol 31 (4) ◽  
pp. 13
Author(s):  
Martin Hyrcza ◽  
Mario Ostrowski ◽  
Sandy Der
Keyword(s):  
Dendritic Cells ◽  
Influenza Virus ◽  
Hiv Infection ◽  
Gene Transcription ◽  
Sendai Virus ◽  
Plasmacytoid Dendritic Cells ◽  
Type I Interferons ◽  
Interferon Response ◽  
Type I ◽  
Type I Ifn

Plasmacytoid dendritic cells (pDCs) are innate immune cells able to produce large quantities of type I interferons (IFN) when activated. Human immunodeficiency virus (HIV)-infected patients show generalized immune dysfunction characterized in part by chronic interferon response. In this study we investigated the role of dendritic cells inactivating and maintaining this response. Specifically we compared the IFN geneactivity in pDCs in response to several viruses and TLR agonists. We hypothesized that 1) the pattern of IFN gene transcription would differ in pDCs treated with HIV than with other agents, and 2) that pDCs from patients from different stages of disease would respond differently to the stimulations. To test these hypotheses, we obtained pDCs from 15 HIV-infected and uninfected individuals and treated freshly isolated pDCs with either HIV (BAL strain), influenza virus (A/PR/8/34), Sendai virus (Cantell strain), TLR7 agonist(imiquimod), or TLR9 agonist (CpG-ODN) for 6h. Type I IFN gene transcription was monitored by real time qPCRfor IFNA1, A2, A5, A6, A8,A17, B1, and E1, and cytokine levels were assayed by Cytometric Bead Arrays forTNF?, IL6, IL8, IL10, IL1?, and IL12p70. pDC function as determined by these two assays showed no difference between HIV-infected and uninfected patients or between patients with early or chronic infection. Specifically, HIV did notinduce type I IFN gene expression, whereas influenza virus, Sendai virus and imiquimod did. Similarly, HIV failed to induce any cytokine release from pDCs in contrast to influenza virus, Sendai virus and imiquimod, which stimulatedrelease of TNF?, IL6, or IL8. Together these results suggest that the reaction of pDCs to HIV virus is quantitatively different from the response to agents such as virus, Sendai virus, and imiquimod. In addition, pDCs from HIV-infected persons have responses similar to pDCs from uninfected donors, suggesting, that the DC function may not be affected by HIV infection.

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