L
Luciana Besedovsky
Researcher at University of Tübingen
Publications - 29
Citations - 1914
Luciana Besedovsky is an academic researcher from University of Tübingen. The author has contributed to research in topics: Cytotoxic T cell & T cell. The author has an hindex of 13, co-authored 22 publications receiving 1219 citations. Previous affiliations of Luciana Besedovsky include Harvard University & University of Lübeck.
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Sleep and immune function
TL;DR: Comparisons of the effects of nocturnal sleep with those of 24-h periods of wakefulness suggest that sleep facilitates the extravasation of T cells and their possible redistribution to lymph nodes, and indicates a specific role of sleep in the formation of immunological memory.
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The Sleep-Immune Crosstalk in Health and Disease
TL;DR: The induction of a hormonal constellation that supports immune functions is one likely mechanism underlying the immune-supporting effects of sleep, and sleep appears to promote inflammatory homeostasis through effects on several inflammatory mediators, such as cytokines.
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Auditory closed-loop stimulation of EEG slow oscillations strengthens sleep and signs of its immune-supportive function
Luciana Besedovsky,Hong-Viet V. Ngo,Hong-Viet V. Ngo,Stoyan Dimitrov,Christoph Gassenmaier,Rainer Lehmann,Jan Born +6 more
TL;DR: Close-loop stimulation of SOs is an easy-to-use tool for probing SWS functions, and might also bear the potential to ameliorate conditions like depression and aging, where disturbed sleep coalesces with specific hormonal and immunological dysregulations.
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Blocking Mineralocorticoid Receptors Impairs, Blocking Glucocorticoid Receptors Enhances Memory Retrieval in Humans
TL;DR: Findings indicate indeed opposing roles of MRs and GRs in memory retrieval, with optimal retrieval at intermediate cortisol levels likely mediated by high MR but concurrently low GR activation.
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Endogenous glucocorticoid receptor signaling drives rhythmic changes in human T-cell subset numbers and the expression of the chemokine receptor CXCR4
TL;DR: It is shown that endogenous cortisol, specifically via GR activation, causes the morning increase in CXCR4 expression and the subsequent extravasation of naive T cells, thus revealing an important immunological function of the morning cortisol rise.