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Autonomous TNF is Critical for in Vivo Monocyte Survival in Steady State and Inflammation
Abstract: Monocytes are circulating mononuclear phagocytes, poised to extravasate to sites of inflammation and differentiate into monocyte-derived macrophages and dendritic cells. Tumor necrosis factor (TNF) and its receptors are up-regulated during monopoiesis and expressed by circulating monocytes, as well as effector monocytes infiltrating certain sites of inflammation, such as the spinal cord, during experimental autoimmune encephalomyelitis (EAE). In this study, using competitive in vitro and in vivo assays, we show that monocytes deficient for TNF or TNF receptors are outcompeted by their wild-type counterpart. Moreover, monocyte-autonomous TNF is critical for the function of these cells, as TNF ablation in monocytes/macrophages, but not in microglia, delayed the onset of EAE in challenged animals and was associated with reduced acute spinal cord infiltration of Ly6Chi effector monocytes. Collectively, our data reveal a previously unappreciated critical cell-autonomous role of TNF on monocytes for their survival, maintenance, and function
Mapping the Origin and Fate of Myeloid Cells in Distinct Compartments of the Eye by Single-cell Profiling
Abstract: Similar to the brain, the eye is considered an immune-privileged organ where tissue-resident macrophages provide the major immune cell constituents. However, little is known about spatially restricted macrophage subsets within different eye compartments with regard to their origin, function, and fate during health and disease. Here, we combined single-cell analysis, fate mapping, parabiosis, and computational modeling to comprehensively examine myeloid subsets in distinct parts of the eye during homeostasis. This approach allowed us to identify myeloid subsets displaying diverse transcriptional states. During choroidal neovascularization, a typical hallmark of neovascular age-related macular degeneration (AMD), we recognized disease-specific macrophage subpopulations with distinct molecular signatures. Our results highlight the heterogeneity of myeloid subsets and their dynamics in the eye that provide new insights into the innate immune system in this organ which may offer new therapeutic targets for ophthalmological diseases
Microglia in Health and Disease: A Unique Immune Cell Population
Microglia are essential for the development and function of the adult brain. Their ontogeny, together with the absence of turnover from the periphery and the singular environment of the central nervous system (CNS), make microglia a unique cell population compared to other tissue-macrophages. The unique properties and functions of microglial cells, such as their role in synaptic pruning or the exceptional capacity to scan the brain parenchyma and rapidly react to its perturbations, have emerged in recent years. In the coming years, understanding how microglia acquire and maintain their unique profiles in order to fulfil distinct tasks in the healthy CNS and how these are altered in disease, ...
Gazeta Lwowska
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Roma A Textband
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Roma B 1 Schülerband
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Agatha Christie’s The Mysterious Affair at Styles in German and Dutch Translation
Agatha Christie is one of the most popular and most translated authors of all time. Yet there is little academic work on her writing. This book sets out to rectify this. No matter where in the world you are, Hercule Poirot is a name that conjures up certain associations. The detailed analysis of the original text, three German and two Dutch translations of The Mysterious Affair at Styles however shows that his depiction differs immensely between the individual texts. In the course of this book, reasons for these differences are found via the analysis of the shifts of status of Agatha Christie as an author of detective fiction and of translations from English in Germany and the Netherlands. During this exploration the discovery will be made that, when translated, escapist literature such as Christie’s detective fiction actually becomes a highly political affair.
Termination Shock
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