Thymic atrophy occurs during viral and bacterial infection, sepsis and endotoxemia, and intestinal damage, which represent a vast number of pathological conditions Using in vitro intact organoid culture of neonatal thymuses, we found that certain combinations of IL12, IL18 and TL1A (the ligand for DR3), results in reduced number of cells in the thymus and the massive egression of myeloid-like cells and NK cells The possible development and exit of other immune cells than T cells in the thymus in any notable amounts is a highly novel finding We hypothesize that the ability to shift the primary output of the neonatal thymus from T cells to myeloid-like cells through pro-inflammatory cytokines exposure may constitute an overlooked, yet fundamental biological function as an adaptation to infection and organ damage Using cutting-edge next-generation single-cell RNA sequencing and state-of-the-art functional assays we aim at phenotyping the ectopic cells exiting the thymus and getting a better understanding of their functionalities In collaboration with the University of Copenhagen, we aim at identifying their role and localization upon commensal colonization using adoptive transfer in germ-free mice We will try to identify the surface markers of these exiting cells and in a final step we will document their egression also in vivo in different models of infection and organ damage