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Molecular Engineering of Zinc Phthalocyanines with Phosphinic Acid Anchoring Groups
Ló,pez‐,Duarte, Ismael,Wang, Mingkui,Humphryx2010,Baker, Robin,Ince, Mine,Martí,nezx2010,Dí,az, M. Victoria,Nazeeruddin, Mohammad K.,Torres, Tomá,s,Grä,tzel, Mich WILEY‐VCH Verlag 2012 Angewandte Chemie Vol.124 No.8
<P><B>Zwei Zinkphthalocyanin‐Photosensibilisatoren</B> mit verschiedenen Phosphinsäure‐Ankergruppen (siehe Schema) wurden synthetisiert. Solarzellen mit diesen Verbindungen verfügen über eine Photostromdichte von (7.6±0.2) mA cm<SUP>−2</SUP> bei geschlossenem Stromkreis, eine Spannung von (559±30) mV bei offenem Stromkreis und einen Füllfaktor von 0.76±0.03; dies entspricht einem Gesamtwirkungsgrad von 3.24 % unter 1 sun.</P>
Ebolavirus VP35 suppresses IFN production from conventional but not plasmacytoid dendritic cells
Leung, Lawrence W,Park, Manx2010,Seong,Martinez, Osvaldo,Valmas, Charalampos,Ló,pez, Carolina B,Basler, Christopher F Nature Publishing Group 2011 Immunology and cell biology Vol.89 No.7
<P>Ebolaviruses naturally infect a wide variety of cells including macrophages and dendritic cells (DCs), and the resulting cytokine and interferon‐α/β (IFN) responses of infected cells are thought to influence viral pathogenesis. The VP35 protein impairs RIG‐I‐like receptor‐dependent signaling to inhibit IFN production, and this function has been suggested to promote the ineffective host immune response characteristic of ebolavirus infection. To assess the impact of VP35 on innate immunity in biologically relevant primary cells, we used a recombinant Newcastle disease virus encoding VP35 (NDV/VP35) to infect macrophages and conventional DCs, which primarily respond to RNA virus infection via RIG‐I‐like pathways. VP35 suppressed not only IFN but also tumor necrosis factor (TNF)‐α secretion, which are normally produced from these cells upon NDV infection. Additionally, in cells susceptible to the activity of VP35, IRF7 activation is impaired. In contrast, NDV/VP35 infection of plasmacytoid DCs, which activate IRF7 and produce IFN through TLR‐dependent signaling, leads to robust IFN production. When plasmacytoid DCs deficient for TLR signaling were infected, NDV/VP35 was able to inhibit IFN production. Consistent with this, VP35 was less able to inhibit TLR‐dependent versus RIG‐I‐dependent signaling <I>in vitro</I>. These data demonstrate that ebolavirus VP35 suppresses both IFN and cytokine production in multiple primary human cell types. However, cells that utilize the TLR pathway can circumvent this inhibition, suggesting that the presence of multiple viral sensors enables the host to overcome viral immune evasion mechanisms.</P>