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- W4313374400 abstract "Abstract Endogenous thymus regeneration is a critical process that enables the restoration of immune competence after damage caused by infection, age and common cancer therapies; however, the molecular mechanisms regulating this process are poorly understood. Previously, we identified that depletion of CD4+CD8+ thymocytes (DPs) after injury precedes the induction of regenerative factors such as BMP4 from endothelial cells (ECs), and IL23 from dendritic cells (DCs), and that the presence of homeostatic apoptotic DPs can suppress BMP4 and IL23. Together with our findings that the metabolic needs of key thymus populations alter drastically following injury due to damage-induced metabolic remodeling, we hypothesize that further to the loss of DP-specific suppression after damage, metabolic dysfunction in DPs triggers mitochondrial-induced pyroptotic cell death, which can directly promote the production of regenerative factors. Here we demonstrate a disruption in glycolytic flux, increased mitochondrial biogenesis, an induction of ROS, and increased cleavage of caspase 1 in murine DPs after damage; key processes that can induce inflammasome activation, pyroptosis and the release of cellular DAMPs such as ATP and HMGB1. Interestingly, these metabolic perturbations were not observed in the regeneration-inducing ECs and DCs, suggesting metabolic stability may facilitate their radio-resistance. Secreted HMGB1 levels are increased in the thymus after damage, and extracellular stimulation of ECs in vitro with ATP increased Bmp4 expression. These studies describe a novel regulatory mechanism of metabolic-mediated tissue regeneration, and have the potential to lead to a superior therapeutic strategy to boost thymic function." @default.
- W4313374400 created "2023-01-06" @default.
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- W4313374400 date "2020-05-01" @default.
- W4313374400 modified "2023-10-01" @default.
- W4313374400 title "Damage-induced pyroptotic cell death facilitates regeneration of the thymus" @default.
- W4313374400 doi "https://doi.org/10.4049/jimmunol.204.supp.79.19" @default.
- W4313374400 hasPublicationYear "2020" @default.
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