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Marie B Iversen - One of the best experts on this subject based on the ideXlab platform.
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mechanisms of type iii interferon Expression
Journal of Interferon and Cytokine Research, 2010Co-Authors: Marie B Iversen, Soren R PaludanAbstract:Type III interferons (IFNs; IFN-Lambda) are antiviral cytokines with type I IFN-like biological functions, including antiviral activity. In this article we review the literature on IFN-Lambda Expression and propose that important differences exist between the mechanisms governing Expression of the different classes of IFNs. Importantly, while IFN-beta is induced by coordinated action of a multifactor enhanceosome, and IFN-alpha Expression is activated by multiple IFN regulatory factor (IRF)-binding cis-promoter elements, the type III IFNs are induced through independent actions of IRFs and nuclear factor-kappaB. Although these differences may appear minor at first glance, we propose that IFN-Lambda Expression is more flexible than IFN-alpha/beta Expression, which could allow Expression of type III IFNs in response to a wider range of stimuli compared with type I IFNs. Moreover, such a mechanism of induction will potentially render Expression of type III IFNs less sensitive to microbial evasion strategies targeting the IRF pathway. Thus, the mechanisms governing type III IFN Expression play an important part in dictating the biology of this antiviral cytokine.
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an important role for type iii interferon ifn Lambda il 28 in tlr induced antiviral activity
Journal of Immunology, 2008Co-Authors: Nina Ank, Marie B Iversen, Christina Bartholdy, Peter Staeheli, Rune Hartmann, Uffe Birk Jensen, Frederik Dagnaeshansen, Allan Randrup Thomsen, Zhi Chen, Harald S HaugenAbstract:Type III IFNs (IFN-Lambda/IL-28/29) are cytokines with type I IFN-like antiviral activities, which remain poorly characterized. We herein show that most cell types expressed both types I and III IFNs after TLR stimulation or virus infection, whereas the ability of cells to respond to IFN-Lambda was restricted to a narrow subset of cells, including plasmacytoid dendritic cells and epithelial cells. To examine the role of type III IFN in antiviral defense, we generated IL-28Ralpha-deficient mice. These mice were indistinguishable from wild-type mice with respect to clearance of a panel of different viruses, whereas mice lacking the type I IFN receptor (IFNAR(-/-)) were significantly impaired. However, the strong antiviral activity evoked by treatment of mice with TLR3 or TLR9 agonists was significantly reduced in both IL-28RA(-/-) and IFNAR(-/-) mice. The type I IFN receptor system has been shown to mediate positive feedback on IFN-alphabeta Expression, and we found that the type I IFN receptor system also mediates positive feedback on IFN-Lambda Expression, whereas IL-28Ralpha signaling does not provide feedback on either type I or type III IFN Expression in vivo. Finally, using bone-marrow chimeric mice we showed that TLR-activated antiviral defense requires Expression of IL-28Ralpha only on nonhemopoietic cells. In this compartment, epithelial cells responded to IFN-Lambda and directly restricted virus replication. Our data suggest type III IFN to target a specific subset of cells and to contribute to the antiviral response evoked by TLRs.
Soren R Paludan - One of the best experts on this subject based on the ideXlab platform.
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mechanisms of type iii interferon Expression
Journal of Interferon and Cytokine Research, 2010Co-Authors: Marie B Iversen, Soren R PaludanAbstract:Type III interferons (IFNs; IFN-Lambda) are antiviral cytokines with type I IFN-like biological functions, including antiviral activity. In this article we review the literature on IFN-Lambda Expression and propose that important differences exist between the mechanisms governing Expression of the different classes of IFNs. Importantly, while IFN-beta is induced by coordinated action of a multifactor enhanceosome, and IFN-alpha Expression is activated by multiple IFN regulatory factor (IRF)-binding cis-promoter elements, the type III IFNs are induced through independent actions of IRFs and nuclear factor-kappaB. Although these differences may appear minor at first glance, we propose that IFN-Lambda Expression is more flexible than IFN-alpha/beta Expression, which could allow Expression of type III IFNs in response to a wider range of stimuli compared with type I IFNs. Moreover, such a mechanism of induction will potentially render Expression of type III IFNs less sensitive to microbial evasion strategies targeting the IRF pathway. Thus, the mechanisms governing type III IFN Expression play an important part in dictating the biology of this antiviral cytokine.
Harald S Haugen - One of the best experts on this subject based on the ideXlab platform.
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an important role for type iii interferon ifn Lambda il 28 in tlr induced antiviral activity
Journal of Immunology, 2008Co-Authors: Nina Ank, Marie B Iversen, Christina Bartholdy, Peter Staeheli, Rune Hartmann, Uffe Birk Jensen, Frederik Dagnaeshansen, Allan Randrup Thomsen, Zhi Chen, Harald S HaugenAbstract:Type III IFNs (IFN-Lambda/IL-28/29) are cytokines with type I IFN-like antiviral activities, which remain poorly characterized. We herein show that most cell types expressed both types I and III IFNs after TLR stimulation or virus infection, whereas the ability of cells to respond to IFN-Lambda was restricted to a narrow subset of cells, including plasmacytoid dendritic cells and epithelial cells. To examine the role of type III IFN in antiviral defense, we generated IL-28Ralpha-deficient mice. These mice were indistinguishable from wild-type mice with respect to clearance of a panel of different viruses, whereas mice lacking the type I IFN receptor (IFNAR(-/-)) were significantly impaired. However, the strong antiviral activity evoked by treatment of mice with TLR3 or TLR9 agonists was significantly reduced in both IL-28RA(-/-) and IFNAR(-/-) mice. The type I IFN receptor system has been shown to mediate positive feedback on IFN-alphabeta Expression, and we found that the type I IFN receptor system also mediates positive feedback on IFN-Lambda Expression, whereas IL-28Ralpha signaling does not provide feedback on either type I or type III IFN Expression in vivo. Finally, using bone-marrow chimeric mice we showed that TLR-activated antiviral defense requires Expression of IL-28Ralpha only on nonhemopoietic cells. In this compartment, epithelial cells responded to IFN-Lambda and directly restricted virus replication. Our data suggest type III IFN to target a specific subset of cells and to contribute to the antiviral response evoked by TLRs.
Nina Ank - One of the best experts on this subject based on the ideXlab platform.
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an important role for type iii interferon ifn Lambda il 28 in tlr induced antiviral activity
Journal of Immunology, 2008Co-Authors: Nina Ank, Marie B Iversen, Christina Bartholdy, Peter Staeheli, Rune Hartmann, Uffe Birk Jensen, Frederik Dagnaeshansen, Allan Randrup Thomsen, Zhi Chen, Harald S HaugenAbstract:Type III IFNs (IFN-Lambda/IL-28/29) are cytokines with type I IFN-like antiviral activities, which remain poorly characterized. We herein show that most cell types expressed both types I and III IFNs after TLR stimulation or virus infection, whereas the ability of cells to respond to IFN-Lambda was restricted to a narrow subset of cells, including plasmacytoid dendritic cells and epithelial cells. To examine the role of type III IFN in antiviral defense, we generated IL-28Ralpha-deficient mice. These mice were indistinguishable from wild-type mice with respect to clearance of a panel of different viruses, whereas mice lacking the type I IFN receptor (IFNAR(-/-)) were significantly impaired. However, the strong antiviral activity evoked by treatment of mice with TLR3 or TLR9 agonists was significantly reduced in both IL-28RA(-/-) and IFNAR(-/-) mice. The type I IFN receptor system has been shown to mediate positive feedback on IFN-alphabeta Expression, and we found that the type I IFN receptor system also mediates positive feedback on IFN-Lambda Expression, whereas IL-28Ralpha signaling does not provide feedback on either type I or type III IFN Expression in vivo. Finally, using bone-marrow chimeric mice we showed that TLR-activated antiviral defense requires Expression of IL-28Ralpha only on nonhemopoietic cells. In this compartment, epithelial cells responded to IFN-Lambda and directly restricted virus replication. Our data suggest type III IFN to target a specific subset of cells and to contribute to the antiviral response evoked by TLRs.
William A Fonzi - One of the best experts on this subject based on the ideXlab platform.
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cloning and characterization of pra1 a gene encoding a novel ph regulated antigen of candida albicans
Journal of Bacteriology, 1998Co-Authors: Maria Sentandreu, Victoria M Elorza, Rafael Sentandreu, William A FonziAbstract:Candida albicans is an opportunistic fungal pathogen of humans. The cell wall of the organism defines the interface between the pathogen and host tissues and is likely to play an essential and pivotal role in the host-pathogen interaction. The components of the cell wall critical to this interaction are undefined. Immunoscreening of a Lambda Expression library with sera raised against mycelial cell walls of C. albicans was used to identify genes encoding cell surface proteins. One of the positive clones represented a candidal gene that was differentially expressed in response to changes in the pH of the culture medium. Maximal Expression occurred at neutral pH, with no Expression detected below pH 6.0. On the basis of the Expression pattern, the corresponding gene was designated PRA1, for pH-regulated antigen. The protein predicted from the nucleotide sequence was 299 amino acids long with motifs characteristic of secreted glycoproteins. The predicted surface localization and N glycosylation of the protein were directly demonstrated by cell fractionation and immunoblot analysis. Deletion of the gene imparted a temperature-dependent defect in hypha formation, indicating a role in morphogenesis. The PRA1 protein was homologous to surface antigens of Aspergillus spp. which react with serum from aspergillosis patients, suggesting that the PRA1 protein may have a role in the host-parasite interaction during candidal infection.
