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Innate lymphoid cells (ILCs) are preferentially localized into barrier tissues where they function in tissue protection but can also contribute to inflammatory diseases. The mechanisms regulating the establishment of ILCs in barrier tissues are poorly understood. Here we show that under steady-state conditions ILCs in skin-draining lymph nodes (sLNs) were continuously activated to acquire regulatory properties and high expression of the chemokine receptor CCR10 for localization into the skin. CCR10+ ILCs promoted the homeostasis of skin-resident T cells and reciprocally, their establishment in the skin required T cell-regulated homeostatic environments. Foxn1-expressing CD207+ dendritic cells were required for the proper generation of CCR10+ ILCs. These observations reveal mechanisms underlying the specific programming and priming of skin-homing CCR10+ ILCs in the sLNs.

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XBP1 confers an important role in protection against oxidative stress in gliomas, potentially via up-regulation of antioxidant molecules such as catalase. Targeting XBP1 may have synergistic effects with ROS inducers on glioma treatment.

Innate lymphoid cells (ILCs) are a newly classified family of immune cells of the lymphoid lineage. While they could be found in both lymphoid organs and non-lymphoid tissues, ILCs are preferentially enriched in barrier tissues such as the skin, intestine, and lung where they could play important roles in maintenance of tissue integrity and function and protection against assaults of foreign agents. On the other hand, dysregulated activation of ILCs could contribute to tissue inflammatory diseases. In spite of recent progress towards understanding roles of ILCs in the health and disease, mechanisms regulating specific establishment, activation, and function of ILCs in barrier tissues are still poorly understood. We herein review the up-to-date understanding of tissue-specific relevance of ILCs. Particularly we will focus on resident ILCs of the skin, the outmost barrier tissue critical in protection against various foreign hazardous agents and maintenance of thermal and water balance. In addition, we will discuss remaining outstanding questions yet to be addressed.

• MicroRNAs (miRNAs) are an important class of non-coding small RNAs that regulate the expression of target genes through mRNA cleavage or translational inhibition. Previous studies have revealed their roles in regulating seed dormancy and germination in model plants such as Arabidopsis thaliana, rice (Oryza sativa) and maize (Zea mays). However, the miRNA response to exogenous gibberellic acid (GA) and abscisic acid (ABA) during seed germination in maize has yet to be explored. • In this study, small RNA libraries were generated and sequenced from maize embryos treated with GA, ABA or double-distilled water as control. • A total of 247 miRNAs (104 known and 143 novel) were identified, of which 45 known and 53 novel miRNAs were differentially expressed in embryos in the different treatment groups. In total, 74 (37 up-regulated and 37 down-regulated) and 55 (23 up-regulated and 32 down-regulated) miRNAs were expressed in response to GA and to ABA, respectively, and a total of 18 known and 38 novel miRNAs displayed differential expression between the GA-and ABA-treated groups. Using bioinformatics tools, we predicted the target genes of the differentially expressed miRNAs. Using GO enrichment and KEGG pathway analysis of these targets, we showed that miRNAs differentially expressed in our samples affect genes encoding proteins involved in the peroxisome, ribosome and plant hormonal signalling pathways. • Our results indicate that miRNA-mediated gene expression influences the GA and ABA signalling pathways during seed germination.

Enteropathogenic Escherichia coli (EPEC) leads to adverse colonic inflammation associated with poor resolution of inflammation and loss of epithelial integrity. Micronutrient trace element selenium (Se) is incorporated into selenoproteins as the 21st amino acid, selenocysteine (Sec). Previous studies have shown that such an incorporation of Sec into the selenoproteome is key for the anti-inflammatory functions of Se in macrophages and other immune cells. An intriguing mechanism underlying the anti-inflammatory and pro-resolving effects of Se stems from the ability of selenoproteins to skew arachidonic acid metabolism from pro-inflammatory mediators, prostaglandin E 2 (PGE 2 ) toward anti-inflammatory mediators derived from PGD 2 , such as 15-deoxy-Δ 12, 14 - prostaglandin J 2 (15d-PGJ 2 ), via eicosanoid class switching of bioactive lipids. The impact of Se and such an eicosanoid-class switching mechanism was tested in an enteric infection model of gut inflammation by C. rodentium , a murine equivalent of EPEC. C57BL/6 mice deficient in Se (Se-D) experienced higher mortality when compared to those on Se adequate (0.08 ppm Se) and Se supplemented (0.4 ppm Se) diets following infection. Decreased survival was associated with decreased group 3 innate lymphoid cells (ILC3s) and T helper 17 (Th17) cells in colonic lamina propria of Se-D mice along with deceased expression of epithelial barrier protein Zo-1. Inhibition of metabolic inactivation of PGE 2 by 15-prostaglandin dehydrogenase blocked the Se-dependent increase in ILC3 and Th17 cells in addition to reducing epithelial barrier integrity, as seen by increased systemic levels of FITC-dextran following oral administration; while 15d-PGJ 2 administration in Se-D mice alleviated the effects by increasing ILC3 and Th17 cells. Mice lacking selenoproteins in monocyte/macrophages via the conditional deletion of the tRNA [Sec] showed increased mortality post infection. Our studies indicate a crucial role for dietary Se in the protection against inflammation following enteric infection via immune mechanisms involving epithelial barrier integrity.

BackgroundThe simultaneous tracking and identification of multiple moving objects encountered in everyday life requires one to correctly bind identities to objects. In the present study, we investigated the role of spatial configuration made by multiple targets when observers are asked to track multiple moving objects with distinct identities.Methodology/Principal FindingsThe overall spatial configuration made by the targets was manipulated: In the constant condition, the configuration remained as a virtual convex polygon throughout the tracking, and in the collapsed condition, one of the moving targets (critical target) crossed over an edge of the virtual polygon during tracking, destroying it. Identification performance was higher when the configuration remained intact than when it collapsed (Experiments 1a, 1b, and 2). Moreover, destroying the configuration affected the allocation of dynamic attention: the critical target captured more attention than did the other targets. However, observers were worse at identifying the critical target and were more likely to confuse it with the targets that formed the virtual crossed edge (Experiments 3–5). Experiment 6 further showed that the visual system constructs an overall configuration only by using the targets (and not the distractors); identification performance was not affected by whether the distractor violated the spatial configuration.Conclusions/SignificanceIn sum, these results suggest that the visual system may integrate targets (but not distractors) into a spatial configuration during multiple identity tracking, which affects the distribution of dynamic attention and the updating of identity-location binding.