Since environmental pollution has exceeded the limit of natural purification, [1] semiconductor-based photocatalytic reactions have attracted intense interest as an effective way of purifying air and water contaminants. [2] Among the various semiconductors, zinc oxide, with a direct wide bandgap (DE = 3.37 eV), is of special importance for the photocatalytic generation of hydrogen peroxide, [3] which can be utilized for the degradation of organic pollutants and the sterilization of bacteria and viruses. [2,4] Due to the fact that a photocatalytic reaction occurs at the interface between catalyst surfaces and organic pollutants, [2] it is highly feasible that the photocatalytic activity of ZnO is strongly dependent on the growth direction of the crystal plane. Such speculation gives us the impetus to explore the relationship between surface orientation of ZnO crystals and their photocatalytic efficiency. However, due to an intrinsic anisotropy in the growth rate v of ZnO,, hexagonal rods elongated along the c-axis have been predominantly synthesized. [5,6] Such an anisotropic tendency in crystal growth makes it difficult to directly probe the relationship between face orientation and photocatalytic activity. Here we report the novel face-tunable synthesis of nano-and microscale ZnO crystals with different ratios of polar to nonpolar faces. With these morphology-controlled crystals, we were able to clearly demonstrate a strong dependence of photocatalytic activity on a specific crystal plane.In Figure 1, we show schematic models for face-tunable synthetic routes to ZnO crystals. The morphologies of the resulting ZnO crystals were investigated with field-emission scanning electron microscopy (FESEM), as shown in Figure 2, and the theoretical surface areas of four different samples, estimated from the FESEM results, are summarized in Table 1.First, hexagonal ZnO nanorods were prepared simply by hydrothermal treatment of dip-coated ZnO nanoparticles on a Si wafer with a uniform size of 4 nm (Fig. 1a).[6a] The corresponding FESEM image of Figure 2a reveals the formation of a dense array of ZnO nanorods with a uniform diameter of 100 nm and a length of 1.5 lm. Due to a one-dimensional nanostructure extended along the [0001] direction, the ZnO nanorods have a larger population of nonpolar {011 0} faces than polar {0001} ones. In order to suppress crystal growth along the [0001] axis, we tried to protect the Zn 2+ -terminated (0001) plane, that is, Zn (0001), through complexation between Zn 2+ ions and citrate ligands. [7] On the basis of this strategy, hexagonal nanoplates with a uniform diameter of 1.0 lm and a thickness of 50 nm were successfully obtained, as can be seen clearly from the FESEM image in Figure 2b. Such formation of nanoplates with a high proportion of polar {0001} planes is surely due to a strong suppression of crystal growth along the [0001] axis with a relative enhancement of crystal growth along the [011 0] direction, as illustrated in Figure 1b. Similarly, the tailored synthesis of diverse ZnO na...

Overactive TH17 responses are tightly linked to the development of autoimmunity, yet the factors that negatively regulate differentiation of this lineage remain unknown. Here, we report that T-bet suppresses the development of the TH17 cell lineage by inhibiting the transcription of Rorc. T-bet interacts with the transcription factor Runx1 and this interaction blocks Runx1-mediated transactivation of Rorc. T-bet residue Tyr304 is required for T-bet-Runx1 complex formation, for blocking Runx1 activity and for inhibiting the TH17 differentiation program. These data reinforce the concept of master regulators that shape immune responses by simultaneously activating one genetic program while silencing the activity of competing regulators in a common progenitor cell.

Mutations affecting RNA splicing factors are the most common genetic alterations in myelodysplastic syndrome (MDS) patients and occur in a mutually exclusive manner. The basis for the mutual exclusivity of these mutations and how they contribute to MDS is not well understood. Here we report that although different spliceosome gene mutations impart distinct effects on splicing, they are negatively selected for when co-expressed due to aberrant splicing and downregulation of regulators of hematopoietic stem cell survival and quiescence. In addition to this synthetic lethal interaction, mutations in the splicing factors SF3B1 and SRSF2 share convergent effects on aberrant splicing of mRNAs that promote nuclear factor κB signaling. These data identify shared consequences of splicing-factor mutations and the basis for their mutual exclusivity.

Foxp3-expressing regulatory T cells (Tregs) are central regulators of immune homeostasis and tolerance. As it has been suggested that proper Treg function is compromised under inflammatory conditions, seeking for a pathway that enhances or stabilizes Treg function is a subject of considerable interest. We report that IL-27, an IL-12 family cytokine known to have both pro- and anti inflammatory roles in T cells, plays a pivotal role in enhancing Treg function to control T cell-induced colitis, a model for inflammatory bowel disease (IBD) in humans. Unlike wild type (WT) Tregs capable of inhibiting colitogenic T cell expansion and inflammatory cytokine expression, IL-27R-deficient Tregs were unable to downregulate inflammatory T cell responses. Tregs stimulated with IL-27 expressed substantially improved suppressive function in vitro and in vivo. IL-27 stimulation of Tregs induced expression of Lag3, a surface molecule implicated in negatively regulating immune responses. Lag3 expression in Tregs was critical to mediate Treg function in suppressing colitogenic responses. Human Tregs also displayed enhanced suppressive function and Lag3 expression following IL-27 stimulation. Collectively, these results highlight a novel function for the IL-27/Lag3 axis in modulating Treg regulation of inflammatory responses in the intestine.

Dysregulated Foxp3 Treg functions result in uncontrolled immune activation and autoimmunity. Therefore, identifying cellular factors modulating Treg functions is an area of great importance. Here, using Treg-specific mice, we report that IL-27 signaling in Foxp3 Tregs is essential for Tregs to control autoimmune inflammation in the central nervous system (CNS). Following experimental autoimmune encephalomyelitis (EAE) induction, Treg-specific mice develop more severe EAE. Consistent with the severe disease, the numbers of IFNγ- and IL-17-producing CD4 T cells infiltrating the CNS tissues are greater in these mice. Treg accumulation in the inflamed CNS tissues is not affected by the lack of IL-27 signaling in Tregs, suggesting a functional defect of Tregs. IL-10 production by conventional CD4 T cells and their CNS accumulation are rather elevated in Treg-specific mice. Analysis with Treg fate-mapping reporter mice further demonstrates that IL-27 signaling in Tregs may control stability of Foxp3 expression. Finally, systemic administration of recombinant IL-27 in Treg-specific mice fails to ameliorate the disease even in the presence of IL-27-responsive conventional CD4 T cells. These findings uncover a previously unknown role of IL-27 in regulating Treg function to control autoimmune inflammation.

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We report on photoluminescence measurements of Mg0.2Zn0.8O∕ZnO∕Mg0.2Zn0.8O multishell layers on ZnO core nanorods. Dominant excitonic emissions in the photoluminescence spectra show a blueshift depending on the ZnO shell layer thickness attributed to the quantum confinement effect in the nanorod heterostructure radial direction. Furthermore, near-field scanning optical microscopy clearly shows sharp photoluminescence peaks from the individual nanorod quantum structures, corresponding to subband levels.