Explore the vast range of titles available.

The separation of melt from crystals is a fundamental process driving the chemical differentiation of magmas and can lead to the formation of pockets of potentially eruptible magmas in highly crystallised magma reservoirs. While geochemical and geophysical evidence exists for the presence of such isolated pockets of eruptible melt, the processes that control their volume and spatial arrangement remain unclear. The Muroto sill in Japan provides an excellent opportunity to study these processes as it is perfectly exposed and shows clear evidence for melt segregation. We collected geochemical and structural data across the sill and performed thermal modelling to quantify extraction timescales and to constrain the range of crystallinity at which melt extraction occurred. Our data and calculations show that the middle–lower portion of the sill experienced melt extraction at crystal fractions between 0.65 and 0.8 over 100–150 years, until magma was too crystalline for further segregation to occur. We propose a new approach that can be used to invert measured geochemical profiles and identify the range of crystallinity at which melt extraction takes place. With this approach, the results we obtain for the Muroto sill can be generalised to magma reservoirs of different sizes and chemistries. Our calculations, and the comparison with natural magmatic systems, show that the volume of melt-rich pockets in a magma reservoir is proportional to the reservoir volume, while their spatial arrangement depends on the physiochemical properties of magmas. The results of this study increase our understanding of the factors controlling the distribution and volume of pockets of eruptible magmas in large magma reservoirs. Our calculations show that eruptible magma in dacitic and rhyolitic magma reservoirs, which are responsible for some of the largest eruptions on Earth, tend to be distributed in lenses of small volume within highly crystallised magma. Such architecture diminishes our capacity of identifying eruptible magma in large magma reservoirs such as Yellowstone using geophysical methods, and jeopardises our capacity of assessing the potential of a reservoir to feed a large eruption.

CD4+ T cells contribute critically to a protective immune response during intestinal infections, but have also been implicated in the aggravation of intestinal inflammatory pathology. Previous studies suggested that T helper type (Th)1 and Th17 cells depend on de novo fatty acid (FA) synthesis for their development and effector function. Here, we report that T-cell-specific targeting of the enzyme acetyl-CoA carboxylase 1 (ACC1), a major checkpoint controlling FA synthesis, impaired intestinal Th1 and Th17 responses by limiting CD4+ T-cell expansion and infiltration into the lamina propria in murine models of colitis and infection-associated intestinal inflammation. Importantly, pharmacological inhibition of ACC1 by the natural compound soraphen A mirrored the anti-inflammatory effects of T-cell-specific targeting, but also enhanced susceptibility toward infection with C. rodentium. Further analysis revealed that deletion of ACC1 in RORγt+ innate lymphoid cells (ILC), but not dendritic cells or macrophages, decreased resistance to infection by interfering with IL-22 production and intestinal barrier function. Together, our study suggests pharmacological targeting of ACC1 as an effective approach for metabolic immune modulation of T-cell-driven intestinal inflammatory responses, but also reveals an important role of ACC1-mediated lipogenesis for the function of RORγt+ ILC.